Parasitic Zoonoses

B. B. Singh DhaliwalPrayag Dutt Juyal

Parasitic Zoonoses

B. B. Singh DhaliwalPrayag Dutt Juyal

Parasitic Zoonoses

123

B. B. Singh DhaliwalSchool of Public Health and ZoonosesGuru Angad Dev Veterinary

and Animal Sciences UniversityLudhiana, PunjabIndia

Prayag Dutt JuyalVeterinary ParasitologyGuru Angad Dev Veterinary

and Animal Sciences UniversityLudhiana, PunjabIndia

ISBN 978-81-322-1550-9 ISBN 978-81-322-1551-6 (eBook)DOI 10.1007/978-81-322-1551-6Springer New Delhi Heidelberg New York Dordrecht London

Library of Congress Control Number: 2013942660

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Preface

The book ‘‘Parasitic Zoonoses’’ is intended for higher undergraduate

and graduate students of zoonoses and public health, veterinary para-

sitology, parasite epidemiology; public health workers; public health

veterinarians; field veterinarians; medical professionals and all others

interested in the subject. The main objective of writing this book is to

provide source of information on zoonotic parasites.

The book describes definition of zoonoses and parasitic zoonoses.

Parasitic zoonoses are the combination of two subjects, i.e., parasitology

and zoonoses where knowledge of both the fields comes into play for the

study of zoonotic parasites. Parasitic zoonoses are the most diversified

group of zoonotic diseases representing all the classes mentioned in

zoonotic diseases classification. They have been classified and discussed

based on etiological agents, transmission cycle, reservoir hosts and

principal host involved along with examples. Important topics such as

food borne, vector borne and occupation-related parasitic zoonoses have

also been covered in the introduction. We have also discussed factors

responsible for emergence of zoonotic parasites viz. climatic change

associated with global warming, increased vector populations, world

tourism, the demand for livestock food products, changing socio-eco-

nomic conditions, poverty, lack of safe drinking water, the large number

of stray animals, changed cooking practices, defecating outdoors, poor

personal hygiene and the high population density in the tropics.

More than 15 protozoa and 50 other parasitic diseases are zoonotic in

nature and all these diseases have been discussed in detail. Each disease

has been divided in different sections viz. synonyms/common names,

etiology, epidemiology, life cycle, mode of transmission, clinical signs in

man and animals, diagnosis and their prevention and control. Life cycle

charts and coloured photographs of these parasites have been included

wherever required. An alphabetical bibliography for every disease has

also been included so that readers have access to further information.

There are few diseases which are rare in occurrence or their zoonotic

potential is still being questioned but they have also been given some

space to update the knowledge of the readers. We hope this book will

prove beneficial to the students and others interested in the subject.

B. B. Singh Dhaliwal

P. D. Juyal

v

Acknowledgments

First of all with great humility, we dedicatedly accord our sincere

gratitude to Almighty God for His benign blessing hand and bestowing

a creative and healthy environment throughout this work.

We feel humbled and acknowledge our indebtedness to the authors of

the research articles whose work has been consulted and cited in this

book. We also thank authors of several source books from where we

took guidance and inspiration for this publication.

We particularly value the mentorship provided by Dr. Alvin A.

Gajadhar and are thankful to professional and technical staff with

Canadian Food Inspection Agency’s Centre for Food Borne and Ani-

mal Parasitology for incessant encouragement and invaluable advice

which enabled us to accomplish the hard task of completing this text

book and making it worth presenting.

We are thankful to faculty members of the School of Public Health

and Zoonoses and Department of Veterinary Parasitology, Guru Angad

Dev Veterinary and Animal Sciences University (GADVASU), Ludhi-

ana (India) for their ever-willing help and scholastic guidance

throughout the writing of this book. We also thank authorities of

GADVASU, Ludhiana, for providing excellent academic atmosphere to

pen this book.

Mere words of acknowledgement will never express the sense of

regards and indebtedness towards our families who are the source of our

strength and inspiration. Their unconditional love, patience, compro-

mises and sacrifice can never be forgotten.

The cooperation and help of Springer India Pvt. Ltd. to bring out this

book is highly appreciated. The authors welcome valuable suggestions

from the readers so as to improve the contents of the book in revised

editions if any published in the future.

B. B. Singh Dhaliwal

P. D. Juyal

vii

Contents

1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11.1 Classification of Parasitic Zoonoses . . . . . . . . . . . . . . . 2

1.1.1 Based on Etiological Agents . . . . . . . . . . . . . 21.1.2 Based on Transmission Cycle . . . . . . . . . . . . 21.1.3 Based on Reservoir Hosts . . . . . . . . . . . . . . . 31.1.4 Based on Principal Host Involved . . . . . . . . . 3

1.2 Animal-Related Parasitic Zoonoses . . . . . . . . . . . . . . . 41.2.1 Livestock-Related Parasitic Zoonoses . . . . . . . 41.2.2 Wildlife-Related Parasitic Zoonoses . . . . . . . . 41.2.3 Domiciliated Animals . . . . . . . . . . . . . . . . . . 51.2.4 Pet Animal-Related Parasitic Zoonoses . . . . . . 51.2.5 Fish, Shellfish and Mollusc-Borne

Parasitic Zoonoses . . . . . . . . . . . . . . . . . . . . 61.3 Occupational Parasitic Zoonoses . . . . . . . . . . . . . . . . . 7

1.3.1 Prevention and Control . . . . . . . . . . . . . . . . . 71.4 Food Borne Parasitic Zoonoses . . . . . . . . . . . . . . . . . . 7

1.4.1 Fish, Shellfish and Mollusc-BorneParasitic Zoonoses . . . . . . . . . . . . . . . . . . . . 10

1.4.2 Meat-Borne Parasitic Zoonoses . . . . . . . . . . . 101.4.3 Water-Borne Parasitic Zoonoses. . . . . . . . . . . 111.4.4 Milk-Borne Parasitic Zoonoses . . . . . . . . . . . 121.4.5 Raw Vegetables/Plant-Borne Parasitic

Zoonoses . . . . . . . . . . . . . . . . . . . . . . . . . . . 131.4.6 Reptile, Amphibian-Borne Parasitic

Zoonoses . . . . . . . . . . . . . . . . . . . . . . . . . . . 131.4.7 Poultry-Related Parasitic Zoonoses . . . . . . . . . 13

1.5 Soil-Transmitted Parasitic Zoonoses . . . . . . . . . . . . . . . 131.5.1 Prevention and Control . . . . . . . . . . . . . . . . . 13

1.6 Vector-Borne Parasitic Zoonoses . . . . . . . . . . . . . . . . . 131.6.1 Prevention and Control . . . . . . . . . . . . . . . . . 14

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

2 Protozoonoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152.1 African Trypanosomiasis. . . . . . . . . . . . . . . . . . . . . . . 15

2.1.1 Common Name/Synonyms . . . . . . . . . . . . . . 152.1.2 History . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152.1.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 16

ix

2.1.4 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 162.1.5 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 162.1.6 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 162.1.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 162.1.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 162.1.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 162.1.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

2.2 Amoebiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 172.2.1 Common Name/Synonyms . . . . . . . . . . . . . . 172.2.2 History . . . . . . . . . . . . . . . . . . . . . . . . . . . . 172.2.3 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 172.2.4 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 172.2.5 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 182.2.6 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 182.2.7 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 182.2.8 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 182.2.9 Clinical Signs in Animals . . . . . . . . . . . . . . . 182.2.10 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 182.2.11 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

2.3 Babesiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182.3.1 Common Name/Synonyms . . . . . . . . . . . . . . 182.3.2 History . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182.3.3 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 192.3.4 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 192.3.5 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 192.3.6 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 192.3.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 192.3.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 192.3.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 192.3.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

2.4 Balantidiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 202.4.1 Common Name/Synonyms . . . . . . . . . . . . . . 202.4.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 202.4.3 History . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212.4.4 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 212.4.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 212.4.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 212.4.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 212.4.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 212.4.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 212.4.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

2.5 Chagas Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212.5.1 Common Name/Synonyms . . . . . . . . . . . . . . 212.5.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 212.5.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 212.5.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 222.5.5 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 222.5.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 222.5.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 22

x Contents

2.5.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 222.5.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

2.6 Cryptosporidiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 222.6.1 Common Name/Synonyms . . . . . . . . . . . . . . 232.6.2 History . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232.6.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 232.6.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 242.6.5 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 242.6.6 Clinical Signs in Animals . . . . . . . . . . . . . . . 242.6.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 242.6.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 242.6.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

2.7 Giardiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 242.7.1 Common Name/Synonyms . . . . . . . . . . . . . . 242.7.2 Etiological Agent . . . . . . . . . . . . . . . . . . . . . 252.7.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 252.7.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 252.7.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 252.7.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 262.7.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 262.7.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 262.7.9 Prevention and Control . . . . . . . . . . . . . . . . . 26

2.8 Leishmaniasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262.8.1 Visceral Leishmaniasis . . . . . . . . . . . . . . . . . 272.8.2 Cutaneous Leishmaniasis. . . . . . . . . . . . . . . . 28

2.9 Sarcocystosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302.9.1 Common Name/Synonyms . . . . . . . . . . . . . . 302.9.2 Etiological Agent . . . . . . . . . . . . . . . . . . . . . 302.9.3 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 302.9.4 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 302.9.5 Clinical Signs in Animals . . . . . . . . . . . . . . . 302.9.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 312.9.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 31

2.10 Toxoplasmosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322.10.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . . . . . 322.10.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 322.10.3 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 322.10.4 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 322.10.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 332.10.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 332.10.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 332.10.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 332.10.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

2.11 Other Protozoan Zoonotic Diseases . . . . . . . . . . . . . . . 332.11.1 Cyclosporiasis . . . . . . . . . . . . . . . . . . . . . . . 332.11.2 Infections Caused by Free-Living Amoebae. . . 352.11.3 Malaria in Non-human Primates. . . . . . . . . . . 35

Contents xi

2.11.4 Microsporidiosis. . . . . . . . . . . . . . . . . . . . . . 352.11.5 Atypical Human Trypanosomiasis . . . . . . . . . 35

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

3 Trematode Zoonoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 413.1 Cercarial Dermatitis . . . . . . . . . . . . . . . . . . . . . . . . . . 41

3.1.1 Common Name/Synonyms . . . . . . . . . . . . . . 413.1.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 423.1.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 423.1.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 423.1.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 423.1.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 423.1.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 423.1.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 433.1.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 433.1.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

3.2 Dicrocoeliasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 433.2.1 Common Name/Synonyms . . . . . . . . . . . . . . 433.2.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 433.2.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 433.2.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 433.2.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 433.2.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 443.2.7 Clinical Signs in Man and Animals . . . . . . . . 443.2.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 443.2.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

3.3 Echinostomiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 453.3.1 Common Name/Synonyms . . . . . . . . . . . . . . 453.3.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 453.3.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 453.3.4 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 453.3.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 453.3.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 453.3.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 453.3.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 463.3.9 Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . 463.3.10 Control and Prevention . . . . . . . . . . . . . . . . . 46

3.4 Fascioliasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 463.4.1 Common Name/Synonyms . . . . . . . . . . . . . . 463.4.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 463.4.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 463.4.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 463.4.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 463.4.6 Clinical Signs in Animals . . . . . . . . . . . . . . . 473.4.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 473.4.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 473.4.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47

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3.5 Fasciolopsiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 473.5.1 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 483.5.2 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 483.5.3 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 483.5.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 483.5.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 483.5.6 Disease in Man . . . . . . . . . . . . . . . . . . . . . . 483.5.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 483.5.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

3.6 Gastrodisciasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483.6.1 Common Name/Synonyms . . . . . . . . . . . . . . 483.6.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 493.6.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 493.6.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 493.6.5 Clinical Signs in Man and Animals . . . . . . . . 493.6.6 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 49

3.7 Heterophyiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493.7.1 Common Name/Synonyms . . . . . . . . . . . . . . 493.7.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 493.7.3 Metagonimiasis . . . . . . . . . . . . . . . . . . . . . . 493.7.4 Heterophyiasis Due to Heterophyes Species. . . 503.7.5 Haplorchiasis . . . . . . . . . . . . . . . . . . . . . . . . 51

3.8 Nanophyetus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 513.8.1 Common Name/Synonyms . . . . . . . . . . . . . . 513.8.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 513.8.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 513.8.4 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 513.8.5 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 523.8.6 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 523.8.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 523.8.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 523.8.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 523.8.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52

3.9 Other Liver Flukes . . . . . . . . . . . . . . . . . . . . . . . . . . . 523.9.1 Clonorchiasis . . . . . . . . . . . . . . . . . . . . . . . . 523.9.2 Opisthorchiasis. . . . . . . . . . . . . . . . . . . . . . . 533.9.3 Metorchiosis (Canadian Liver Fluke) . . . . . . . 53

3.10 Paragonimiasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533.10.1 Common Name/Synonyms . . . . . . . . . . . . . . 533.10.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 543.10.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 543.10.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 543.10.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 543.10.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 543.10.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 553.10.8 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 553.10.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 563.10.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56

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3.11 Schistosomiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 563.11.1 Common Name/Synonyms . . . . . . . . . . . . . . 563.11.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 563.11.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 563.11.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 563.11.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 573.11.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 573.11.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 583.11.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 583.11.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 583.11.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58

4 Cestode Zoonoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 654.1 Coenurosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

4.1.1 Common Name/Synonyms . . . . . . . . . . . . . . 664.1.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 664.1.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 664.1.4 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 664.1.5 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 664.1.6 Clinical Signs in Animals . . . . . . . . . . . . . . . 674.1.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 674.1.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

4.2 Diphyllobothriasis . . . . . . . . . . . . . . . . . . . . . . . . . . . 674.2.1 Common Name/Synonyms . . . . . . . . . . . . . . 674.2.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 674.2.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 674.2.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 684.2.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 684.2.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 684.2.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 684.2.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 684.2.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68

4.3 Dipylidiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 684.3.1 Common Name/Synonyms . . . . . . . . . . . . . . 684.3.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 694.3.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 694.3.4 Life Cycle and Transmission in Man . . . . . . . 704.3.5 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 704.3.6 Clinical Signs in Animals . . . . . . . . . . . . . . . 704.3.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 704.3.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71

4.4 Echinococcosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 714.4.1 Common Name/Synonyms . . . . . . . . . . . . . . 714.4.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 714.4.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 714.4.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 714.4.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 714.4.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 72

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4.4.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 724.4.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 734.4.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73

4.5 Sparganosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 744.5.1 Common Name/Synonyms . . . . . . . . . . . . . . 744.5.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 744.5.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 744.5.4 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 744.5.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 744.5.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 754.5.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 754.5.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 754.5.9 Prevention and Control . . . . . . . . . . . . . . . . . 75

4.6 Taeniasis and Cysticercosis . . . . . . . . . . . . . . . . . . . . . 764.6.1 Common Name/Synonyms . . . . . . . . . . . . . . 764.6.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 764.6.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 764.6.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 764.6.5 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 764.6.6 Clinical Signs in Animals . . . . . . . . . . . . . . . 774.6.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 774.6.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78

4.7 Other Cestode Zoonoses . . . . . . . . . . . . . . . . . . . . . . . 784.7.1 Bertiellosis . . . . . . . . . . . . . . . . . . . . . . . . . 784.7.2 Hymenolepiosis . . . . . . . . . . . . . . . . . . . . . . 794.7.3 Inermicapsiferosis. . . . . . . . . . . . . . . . . . . . . 794.7.4 Mesocestoidosis . . . . . . . . . . . . . . . . . . . . . . 794.7.5 Raillietinosis . . . . . . . . . . . . . . . . . . . . . . . . 79

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79

5 Nematode Zoonoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 835.1 Acanthocephalus . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83

5.1.1 Common Name/Synonyms . . . . . . . . . . . . . . 835.1.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 835.1.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 845.1.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 845.1.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 845.1.6 Clinical Signs in Man and Animals . . . . . . . . 845.1.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 855.1.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85

5.2 Angiostrongylosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . 855.2.1 Common Name/Synonyms . . . . . . . . . . . . . . 855.2.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 855.2.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 855.2.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 855.2.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 855.2.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 865.2.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 86

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5.2.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 865.2.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86

5.3 Anisakiosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 865.3.1 Common Name/Synonyms . . . . . . . . . . . . . . 875.3.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 875.3.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 875.3.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 875.3.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 875.3.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 875.3.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 875.3.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 885.3.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88

5.4 Ascariosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 885.4.1 Common Name/Synonyms . . . . . . . . . . . . . . 885.4.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 885.4.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 895.4.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 895.4.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 895.4.6 Clinical Signs in Man and Animals . . . . . . . . 895.4.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 895.4.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89

5.5 Baylisascariasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 895.5.1 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 895.5.2 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 905.5.3 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 905.5.4 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 905.5.5 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 905.5.6 Clinical Signs in Animals . . . . . . . . . . . . . . . 905.5.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 905.5.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90

5.6 Capillariasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 915.6.1 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 915.6.2 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 915.6.3 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 915.6.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 915.6.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 925.6.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 925.6.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 925.6.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 925.6.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92

5.7 Cutaneous Larva Migrans . . . . . . . . . . . . . . . . . . . . . . 925.7.1 Common Name/Synonyms . . . . . . . . . . . . . . 925.7.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 925.7.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 925.7.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 935.7.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 935.7.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 935.7.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 935.7.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 93

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5.7.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 935.7.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93

5.8 Dioctophymosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 935.8.1 Common Name/Synonyms . . . . . . . . . . . . . . 935.8.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 935.8.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 935.8.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 945.8.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 945.8.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 945.8.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 945.8.8 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 945.8.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 945.8.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94

5.9 Dracunculiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 945.9.1 Common Name/Synonyms . . . . . . . . . . . . . . 945.9.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 955.9.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 955.9.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 955.9.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 955.9.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 955.9.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 955.9.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 955.9.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 955.9.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 96

5.10 Gnathostomiasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 965.10.1 Common Name/Synonyms . . . . . . . . . . . . . . 965.10.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 965.10.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 965.10.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 965.10.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 965.10.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 975.10.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 975.10.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 975.10.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 975.10.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97

5.11 Gongylonemosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 975.11.1 Common Name/Synonyms . . . . . . . . . . . . . . 975.11.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 975.11.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 985.11.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 985.11.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 985.11.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 985.11.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 995.11.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 995.11.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 995.11.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99

5.12 Lagochilascariosis . . . . . . . . . . . . . . . . . . . . . . . . . . . 995.12.1 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 995.12.2 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 99

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5.12.3 Reservoir and Transmission of the Disease . . . 995.12.4 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 995.12.5 Disease in Man . . . . . . . . . . . . . . . . . . . . . . 1005.12.6 Disease in Animals. . . . . . . . . . . . . . . . . . . . 1005.12.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1005.12.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100

5.13 Mammomonogamus . . . . . . . . . . . . . . . . . . . . . . . . . . 1005.13.1 Common Name/Synonyms . . . . . . . . . . . . . . 1005.13.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1005.13.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1005.13.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1015.13.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1015.13.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1015.13.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1015.13.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1015.13.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1015.13.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101

5.14 Micronemosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1015.14.1 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1015.14.2 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1015.14.3 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1015.14.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1025.14.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1025.14.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1025.14.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 1025.14.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1025.14.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

5.15 Oesophagostomiasis . . . . . . . . . . . . . . . . . . . . . . . . . . 1025.15.1 Common Name/Synonyms . . . . . . . . . . . . . . 1025.15.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1025.15.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1025.15.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1035.15.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1035.15.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1035.15.7 Clinical Signs in Man and Animals . . . . . . . . 1035.15.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1035.15.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103

5.16 Strongyloidiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1035.16.1 Common Name/Synonyms . . . . . . . . . . . . . . 1035.16.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1035.16.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1045.16.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1045.16.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1045.16.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1045.16.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1045.16.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1045.16.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1045.16.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104

xviii Contents

5.17 Thelaziasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1045.17.1 Common Name/Synonyms . . . . . . . . . . . . . . 1055.17.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1055.17.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1055.17.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1055.17.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1055.17.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1055.17.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1055.17.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1055.17.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1055.17.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105

5.18 Trichinosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1055.18.1 Common Name/Synonyms . . . . . . . . . . . . . . 1065.18.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1065.18.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1065.18.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1065.18.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1065.18.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1065.18.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1075.18.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1075.18.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1075.18.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107

5.19 Trichostrongylosis . . . . . . . . . . . . . . . . . . . . . . . . . . . 1085.19.1 Common Name/Synonyms . . . . . . . . . . . . . . 1085.19.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1085.19.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1095.19.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1095.19.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1095.19.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1095.19.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1095.19.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1095.19.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1095.19.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109

5.20 Trichuriasis of Animal Origin . . . . . . . . . . . . . . . . . . . 1095.20.1 Common Name/Synonyms . . . . . . . . . . . . . . 1095.20.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1095.20.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1105.20.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1105.20.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1105.20.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1105.20.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1105.20.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1105.20.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1105.20.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110

5.21 Visceral Larva Migrans . . . . . . . . . . . . . . . . . . . . . . . 1105.21.1 Common Name/Synonyms . . . . . . . . . . . . . . 1105.21.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1105.21.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1115.21.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 111

Contents xix

5.21.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1115.21.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1115.21.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1115.21.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1115.21.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1115.21.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111

5.22 Zoonotic Ancylostomiasis . . . . . . . . . . . . . . . . . . . . . . 1125.22.1 Common Name/Synonyms . . . . . . . . . . . . . . 1125.22.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1125.22.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1125.22.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1135.22.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1135.22.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1135.22.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1135.22.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1135.22.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1135.22.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113

5.23 Zoonotic Filariasis . . . . . . . . . . . . . . . . . . . . . . . . . . . 1145.23.1 Common Name/Synonyms . . . . . . . . . . . . . . 1145.23.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1145.23.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1145.23.4 Reservoir. . . . . . . . . . . . . . . . . . . . . . . . . . . 1145.23.5 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1145.23.6 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1145.23.7 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1145.23.8 Clinical Signs in Animals . . . . . . . . . . . . . . . 1155.23.9 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1155.23.10 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

6 Arthropod Zoonoses. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1236.1 Myiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123

6.1.1 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1236.1.2 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1246.1.3 Clinical Signs in Animals . . . . . . . . . . . . . . . 1246.1.4 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1246.1.5 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1246.1.6 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124

6.2 Pentastomiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1246.2.1 Common Name/Synonyms . . . . . . . . . . . . . . 1246.2.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1246.2.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1256.2.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1256.2.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1256.2.6 Clinical Signs in Man . . . . . . . . . . . . . . . . . . 1256.2.7 Clinical Signs in Animals . . . . . . . . . . . . . . . 1256.2.8 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1256.2.9 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125

xx Contents

6.3 Tungiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1266.3.1 Synonyms . . . . . . . . . . . . . . . . . . . . . . . . . . 1266.3.2 Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . 1266.3.3 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . 1266.3.4 Transmission . . . . . . . . . . . . . . . . . . . . . . . . 1266.3.5 Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . 1266.3.6 Clinical Signs in Man and Animals . . . . . . . . 1266.3.7 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . 1266.3.8 Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126

6.4 Zoonotic Dermatitis . . . . . . . . . . . . . . . . . . . . . . . . . . 1266.4.1 Zoonotic Scabies . . . . . . . . . . . . . . . . . . . . . 1266.4.2 Tick Infestations. . . . . . . . . . . . . . . . . . . . . . 1276.4.3 Dermatitis Due to Acarid Parasites Belonging

to Families Cheyletiellidae, Dermanyssidaeand Macronyssidae . . . . . . . . . . . . . . . . . . . . 128

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129

About the Authors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133

Contents xxi

1Introduction

Abstract

Parasitism is basically association between two species: Parasite (firstspecies) and the host (second species). Parasitic diseases cause significantproblems in the developing world. At present, there are more than 15protozoa and 50 other parasitic diseases that are zoonotic in nature.Zoonotic parasites are important due to their human and animal health,food safety and economic concerns. Emergence and re-emergence ofmany zoonotic parasites have been reported across the globe. Contam-inated water and food significantly increase the transmission of theseparasites. Factors influencing prevalence of these parasites includeresurgence in vector population, climate change coupled with globalwarming, international food trade, poverty and lack of safe drinkingwater in non-industrialised countries, etc. Most of the animals which livein close contact with man could harbour and transmit zoonotic parasitesto human beings. Livestock, pets, domiciliated, wild animals, fish andsome other animals; all of them could transmit zoonotic parasites. Anupdate on current status of zoonotic parasites has been provided.

Parasitism is basically association between twospecies: Parasite (first species) and the host(second species). In this association, parasitelives on the host or its tissue for certain periods oftime. This association can be of different types,viz. symbiosis, commensalism, mutualism,phoresis, predation or parasitism. Such hostparasite relationship could lead to pathologicaldisorders and disease in the host. In animals andman, many important diseases occur due to par-asites. Parasitic diseases cause significant prob-lems particularly in the developing world.Approximately 370 parasitic species (300 hel-minths and 70 protozoa) have been found inhuman beings (Ashford and Crewe 1998;

Cox 2002). Out of these, some parasites causeimportant parasitic diseases in man. The para-sites are generally classified under the categories:Protozoa, helminths and arthropods (Fig. 1.1).

At present, there are more than 15 protozoaand 50 other parasitic diseases that are zoonoticin nature. Zoonotic parasites are important dueto their human and animal health, food safetyand economic concerns.

As per World Health Organization (Acha andSzyfres 2006), zoonoses are defined as ‘‘thosediseases and infections (the agents of) which arenaturally transmitted between (other) vertebrateanimals and man’’. Many new zoonotic diseaseshave been recognised in the recent past to further

B. B. S. Dhaliwal and P. D. Juyal, Parasitic Zoonoses,DOI: 10.1007/978-81-322-1551-6_1, � Springer India 2013

1

expand the existing list of zoonotic diseases.Zoonotic parasitology is the study of phenome-non of parasites which are zoonotic in nature. Inother words, parasitic zoonoses are the combi-nation of two subjects: Parasitology and zoono-ses where knowledge of both the fields comesinto play for study of zoonotic parasites.

Parasitic zoonotic diseases are prevalentworldwide. First reports, emergence andre-emergence of zoonotic parasites, have beenrecorded in human and animal populations in thepast decades (Singh et al. 2010). Importantfactors that influence the occurrence of zoonoticparasites, particularly in the developing world,include climate change and global warming,vector populations, poverty, lack of safe drink-ing water, presence of stray animals, defecatingoutdoors, poor personal hygiene and the highpopulation density (Singh et al. 2011).

Parasitic zoonoses can be classified intodifferent categories as in case of zoonoses(Schwabe 1984). Parasitic zoonoses are the mostdiversified group of zoonotic diseases repre-senting all classes of zoonotic diseases classifiedon different bases.

1.1 Classification of ParasiticZoonoses

1.1.1 Based on Etiological Agents

1. Protozoonoses: cryptosporidiosis, giardiasis,toxoplasmosis, etc.

2. Trematode zoonoses: clonorchiosis, para-gonimiasis, etc.

3. Cestode zoonoses: hydatidosis, taeniosis,cysticercosis, etc.

4. Nematode zoonoses: larva migrans, trichi-nosis, zoonotic ancylostomiasis, etc.

5. Arthropod zoonoses: myiases, zoonotic sca-bies, etc.

1.1.2 Based on Transmission Cycle

The parasitic zoonotic diseases can be classifieddepending upon the life cycle of the zoonoticpathogens.

1. Direct parasitic zoonoses: The parasite istransmitted by direct contact or indirectly

Fig. 1.1 Classification of parasites

2 1 Introduction

through food, e.g. scabies, trichinellosis,giardiasis, etc.

2. Cyclozoonoses: The diseases caused byzoonotic parasites require two or more ver-tebrate hosts to complete life cycle of theparasite. Cyclozoonoses are further classi-fied under two categories:(a) Obligatory cyclozoonoses: Human

beings must act as host to complete lifecycle of the parasite, e.g. Taenia soliumand Taenia saginata taeniosis.

(b) Non-obligatory cyclozoonoses: Humanbeings are not required to completelifecycle of the parasite but could act asaccidental host, e.g. human hydatidosis.

3. Metazoonoses: The diseases caused bythose zoonotic parasites which require bothvertebrate and invertebrate species tocomplete life cycle of the parasite. Meta-zoonoses are further classified under fourcategories:(a) Metazoonoses type I: The diseases caused

by those zoonotic parasites which requireone invertebrate and one vertebrate host,e.g. Dipylidium caninum dipylidiasis.

(b) Metazoonoses type II: The diseasescaused by those zoonotic parasiteswhich require two invertebrate and onevertebrate hosts, e.g. paragonimiasis.

(c) Metazoonoses type III: The diseasescaused by those zoonotic parasiteswhich require one invertebrate and twovertebrate hosts, e.g. clonorchiosis.

(d) Metazoonoses type IV: The diseasescaused by those zoonotic parasiteswhich require transovarian transmis-sion, e.g. Babesia divergens babesiosis.

4. Saprozoonoses: The diseases caused bythose zoonotic parasites which require non-animate material in addition to their hostsfor completion of life cycle. Saprozoonosesare further classified under three categories:(a) Saproanthropozoonoses: Animals princi-

pally act as reservoir host and the etio-logical agents are transmitted from

animals to man through inanimate mate-rial, e.g. cutaneous larva migrans, myiasis.

(b) Saproamphixenoses: Both animals andhumans could act as reservoir hosts andthe etiological agents are transmittedthrough inanimate objects, e.g. probablymicronemosis.

(c) Saprometanthropozoonoses: Sapromet-anthropozoonoses require vertebratehost, invertebrate host and inanimatesubstance for transmission of disease,e.g. fasciolosis.

1.1.3 Based on Reservoir Hosts

1. Anthropozoonoses: The diseases in whichanimals act as reservoir hosts and humansbecome accidentally infected, e.g. hydatido-sis, visceral larvae migrans.

2. Zooanthroponoses: These diseases are nor-mally present in humans but could be trans-mitted to animals, e.g. amoebosis.

3. Amphixenosis: The diseases in which bothman and animals could act as reservoir hosts,e.g. clonorchiosis.

1.1.4 Based on Principal HostInvolved

1. Cattle-related parasitic zoonoses: T. saginatataeniosis, cryptosporidiosis.

2. Sheep-related parasitic zoonoses: fasciolosis,hydatidosis.

3. Pig-related parasitic zoonoses: ascariasis,swine taeniosis.

4. Fish-related parasitic zoonoses: diphyllo-bothriosis.

5. Dog-related parasitic zoonoses: ancylosto-miasis, echinococcosis.

6. Cat-related parasitic zoonoses: toxoplas-mosis.

7. Racoon-related parasitic zoonoses: baylisa-scariosis.

1.1 Classification of Parasitic Zoonoses 3

1.2 Animal-Related ParasiticZoonoses

Most of the animals which are in close contactwith man could harbour and transmit zoonoticparasites to human beings. Livestock, pets,domiciliated, wild animals, fish and some otheranimals, all of them could transmit zoonoticparasites (Parija 1990).

1.2.1 Livestock-Related ParasiticZoonoses

Livestock is an essential component of humanactivities particularly for dairy farmers, veteri-narians and other related occupations. The foodof animal origin, viz. meat, milk and theirproducts are essential components of humandiet. The human and livestock populations livein close association with each other. This closeassociation and dependence for food can resultin transmission of zoonotic parasites whenproper hygienic measures are not taken. Thesediseases can be transmitted either through food,contaminated water or by vector population.

Livestock transmitted parasitic zoonoses canbe classified either on the basis of speciesinvolved or on the basis of mode of their trans-mission (Figs. 1.2, 1.3, 1.4, 1.5, 1.6, 1.7).

Based on the animal species involved, theycan be classified into:1. Cattle-related parasitic zoonoses: B. divergens

babesiosis, cryptosporidiosis, sarcocystosis,fasciolosis, T. saginata taeniosis.

2. Pig-related parasitic zoonoses: balantidiasis,sarcocystosis, toxoplasmosis, gastrodiscoi-dosis, T. solium taeniosis, ascariosis, gna-thostomosis, trichinosis.

3. Sheep-related parasitic zoonoses: toxoplas-mosis, fasciolosis.

4. Goat related parasitic zoonoses: toxoplas-mosis.

1.2.2 Wildlife-Related ParasiticZoonoses

Human beings, particularly hunters, forestworkers, agricultural workers, army personnel,tourists and other related occupational workers,may be exposed to wild animal-related parasiticzoonoses. The wild animal reservoir hosts ofsome diseases may also enter human anddomestic animal habitations leading to theirtransmission and occurrence in human beings.

Examples of wildlife-related parasiticzoonoses

Opossums (Didelphis albiventris, Didelphis mar-supialis): Trypanosoma cruzi trypanosomosis.

Fig. 1.2 Zoonoticparasites of pig

4 1 Introduction

Monkeys: malaria of simian origin.Wild cats: toxoplasmosis.Wild felids: baylisascariosis.Wild boar: trichinosis.Racoons: baylisascariosis.

1.2.3 Domiciliated Animals

Domiciliated animals live in close associationwith human habitats. They may be partly depen-dent on man for food and shelter. Resultantly, theycan always transmit zoonotic parasitic diseases.

Examples of Domiciliated animal-relatedparasitic zoonoses

Rodents: Babesia microti babesiosis, leishmani-osis, angiostrongylosis.

Reptile/amphibian borne: sparganosis, gnathos-tomosis.

1.2.4 Pet Animal-Related ParasiticZoonoses

Pet animals are kept by man for companionship,security and enjoyment. Dogs and cats are themost common and popular pets kept worldwide.

Fig. 1.3 Zoonoticparasites of cattle

Fig. 1.4 Zoonoticparasites of sheep and goat

1.2 Animal-Related Parasitic Zoonoses 5

Poor animal hygiene may result in transmissionof such diseases to the human population.

Examples of Pet animal-related parasiticzoonoses

Dogs: T. cruzi trypanosomosis, leishmaniosis,diplydiasis, echinococcosis, cutaneous larvamigrans, gnathostomosis, toxocariasis.

Cats: T. cruzi trypanosomosis, toxoplasmosis,diplydiasis, cutaneous larvae migrans,gnathostomosis.

1.2.5 Fish, Shellfish and Mollusc-Borne Parasitic Zoonoses

Fish are aquatic vertebrates and are essentialcomponent of human diet. Fish is an importantsource of protein for man. Ingestion of con-taminated raw fish may transmit importantzoonotic infections.

Examples of Fish, shellfish, craband mollusc-borne parasitic zoonoses

Fig. 1.5 Zoonoticparasites of rodents

Fig. 1.6 Zoonoticparasites of cat

6 1 Introduction

Angiostrongylosis, paragonimiasis, anisakiosis,clonorchiosis, diphyllobothriosis, echinosto-mosis, Heterophyes heterophyes infections,Haplorchis spp. infections, Matagonimusyokogamai infections (Figs. 1.8, 1.9).

1.3 Occupational ParasiticZoonoses

Occupational parasitic zoonoses are the zoonoticparasitic diseases which may occur due to theoccupational environment in persons relatedwith specific occupation. There is increased riskof contacting such diseases in persons workingin specific occupational areas. In addition tooccupational zoonoses, immunocompromisedpersons are always at higher risk of beinginfected with zoonotic parasites such as Cryp-tosporidium parvum, Toxoplasma gondii, etc.There is also a strong correlation between

occurrence of zoonotic babesiosis among sple-nectomized individuals (Fig. 1.10).

1.3.1 Prevention and Control

• To generate better awareness regardingtransmission and prevention of occupationalzoonoses among related occupational groups.

• Monitoring and surveillance of occupationallyrelated zoonotic parasites among risk groups.

• Control of such disease in their animal hosts.

1.4 Food Borne Parasitic Zoonoses

The food animals, viz. cattle, buffalo, sheep,goat and pigs consume fodder crops and convertthem into animal protein. The meat from theseanimals is an important source of protein andnutrients (Gracey and Collins 1992). Fish and

Fig. 1.7 Zoonoticparasites of dog

1.2 Animal-Related Parasitic Zoonoses 7

other sea foods also make a vital contribution toprovide essential nourishment for human popu-lation. The meat of wild animals is also used as a

part of human diet in many parts of the world.Poultry are another important meat producingspecies. Besides fish and meat, milk and rawvegetables also form important components ofhuman food. Food and water are the twoessential components of human diet. The food ofanimal origin is a rich source of proteins, energy,vitamins and minerals. The food especially ofanimal origin is essential for growth and devel-opment of human beings.

However, presence of zoonotic parasites insuch food and contaminated water could lead totheiroccurrenceinmanandanimals.Transmissionof zoonoses of parasitic origin through food haspublic health as well as socio-economic signifi-cance (Slifko et al. 2000). Transmission of zoo-notic parasites through contaminated water, food,plants, vegetables and soil assumes great impor-tance (Slifko et al. 2000; Zhou et al. 2008). Foodsecurity is an important issue due to increasinghuman populations, income levels, changing foodpreferences and urbanisation. The demand forfood of animal origin is increasing worldwide.

Food and water act as an important route oftransmission for parasites from one host toanother. Food and water are also important fortransmission of parasites which require morethan one host to complete their life cycle

Fig. 1.8 Zoonotic parasites of some other animals

Fig. 1.9 Zoonotic parasites of man

8 1 Introduction

(Bhatia 1991). The important parasites trans-mitted through food and water includes T. soli-um, Echinococcus granulosus, T. gondii, etc.Parasites exploit behavioural patterns of theirhosts for further transmission among animals andhumans (Gajadhar et al. 2006). Further, parasitelife cycle stages such as eggs and oocysts havethe ability to resist and survive adverse envi-ronmental conditions (Gajadhar et al. 2006).Many factors have lead to an increased risk forthe occurrence of food borne zoonotic parasites.Climate change and increased food trade havemanifold increased the risk of food borne para-sitic zoonoses. Increased demand for animal fooddue to rapid urbanisation, increase in humanpopulation and high income indicates need formore emphasis on food safety issues (Gajadhar

et al. 2006). Many emerging zoonotic parasitesare food borne in nature (WHO 2002)(Fig. 1.11).

Prevention and control strategies shouldinclude use of advanced serological and molec-ular diagnostic techniques, continuous monitor-ing of zoonotic parasites, health education,social and economic development particularly inthe developing world; and prompt treatment ofcases (Dorny et al. 2009). Many importantparasites shed their eggs in the faeces whichserve as an important source of infection leadingto contamination of environment particularlywater and food supplies (Slifko et al. 2000).One or more life cycle stages of the parasitecan transmit the infection. For example, inges-tion of only infectious oocysts leads to

Fig. 1.10 Occupational parasitic zoonoses

Fig. 1.11 Food borne parasitic zoonoses

1.4 Food Borne Parasitic Zoonoses 9

cryptosporidiosis, whereas both oocysts andtissue cysts of T. gondii can cause infection inman (Slifko et al. 2000).

1.4.1 Fish, Shellfish and Mollusc-Borne Parasitic Zoonoses

Fish and related zoonoses can be classified intotrematode, cestode and nematode zoonoses.Trematode diseases can be further sub-classifiedinto liver and intestinal flukes. As perWHO (1995), fish-borne trematodes infect morethan 18 million people and globally more thanhalf a billion people are at risk from these dis-eases (Chai et al. 2005) (Fig. 1.12).

1.4.1.1 Prevention and Control• Avoid eating raw or improperly cooked fish.• Interruption in the transmission cycle of the

parasite.• Health education and environmental

sanitation.• Use of clean water in slaughtering operations

to avoid contamination with other water-bornezoonotic parasites.

1.4.2 Meat-Borne Parasitic Zoonoses

Many important parasitic zoonotic diseases aremeat-borne in nature, e.g. toxoplasmosis, taeni-osis, trichinellosis, etc. Most of the food pro-ducing animals (except poultry), viz. cattle,

Fig. 1.12 Fish-shellfish and mollusc-borne parasitic zoonoses

Fig. 1.13 Meat-borne parasitic zoonoses

10 1 Introduction

buffalo, pig, sheep and goat could transmitzoonotic parasites. Meat-borne parasitic diseasescan be further classified either on the basis ofanimal host involved or into protozoan, trema-tode, cestode and nematode meat-borne parasiticzoonoses (Figs. 1.13, 1.14).

1.4.2.1 Prevention and Control• Avoid consumption of raw or under cooked

meat.• Provide safe food and water to livestock.

• Use of best hygienic practices during slaugh-tering operations to avoid contamination withother water-borne zoonotic parasites.

1.4.3 Water-Borne Parasitic Zoonoses

These parasites are prevalent worldwide andpose a significant threat particularly in thedeveloping world (Gajadhar and Allen 2004).The non-availability of clean and hygienicdrinking water is an important risk in thedeveloping world. The parasite stages that canbe transmitted through water range from uni-cellular amoebae to complex metazoans such astrematodes and cestodes (Gajadhar andAllen 2004). The life cycle stages of these par-asites are well adapted for their survival in theenvironment and further dissemination by water(Gajadhar and Allen 2004). Many importantzoonotic parasites such as C. parvum, T. gondii,could be transmitted through contaminatedwater. Transport hosts such as swine can also

Fig. 1.14 Meat-borne parasitic zoonoses

Fig. 1.15 Water-borne parasitic zoonoses

Fig. 1.16 Vector-borne parasitic zoonoses

1.4 Food Borne Parasitic Zoonoses 11

play an important role in collection and con-centration of resistant exogenous stages (Gaja-dhar and Allen 2004) of many parasites.Important water-borne parasitic zoonoses can beclassified through protozoa, trematode and ces-tode zoonoses, but protozoan zoonoses are morecommon and significant (Fig. 1.15).

1.4.3.1 Prevention and Control• Use properly filtered water for drinking

purpose.• Routine monitoring of drinking water.

• Regular deworming of reservoir and animalhosts.

• Avoid surface contamination of swimmingpools.

1.4.4 Milk-Borne Parasitic Zoonoses

Although milk is considered as safer food inrelation to zoonotic parasites, but milk of cap-rine and ovine can cause toxoplasmosis in man ifthe animal is infected with the disease and rawmilk is consumed. Additionally, external faecal

Fig. 1.17 Classification of vector-borne parasitic zoonoses as per Colwell et al. (2011)

12 1 Introduction

contamination during or after milking couldpose additional risks for transmission of someimportant zoonotic parasites.

1.4.5 Raw Vegetables/Plant-BorneParasitic Zoonoses

The role of raw vegetables/salad in transmissionof zoonotic parasites gets attention particularly incases of neurocysticercosis in humans wherehuman sewage has been used for irrigation pur-poses for farmland used to grow vegetables and ithas been found to be an important risk fortransmission of the disease. Fasciolosis is anotherimportant disease which can be transmittedthrough ingestion of contaminated plants. Thecontamination of vegetables could also help intransmission of parasites such as Ascaris suumand Toxocara species (Slifko et al. 2000).

1.4.6 Reptile, Amphibian-BorneParasitic Zoonoses

Sparganosis and Gnathostomosis are twoimportant cestode and nematode diseases,respectively which can occur in human beingsdue to consumption of raw or under cookedreptiles or amphibians.

1.4.7 Poultry-Related ParasiticZoonoses

No zoonotic parasites are present in poultry meatand it is generally free from zoonotic parasitesexcept that clean water should be used inslaughtering operations. However, free rangingchicken could serve as important reservoir fortoxoplasmosis. A recent study has demonstratedthat poultry may serve as a minor reservoir forfish borne trematodes (Anh et al. 2010).

1.5 Soil-Transmitted ParasiticZoonoses

Soil-transmitted zoonotic parasites include hel-minth infections, viz. ascariosis due to Ascarislumbricoides, hookworm infections dueto Ancylostoma spp. and toxocarosis due toToxocara canis and Toxocara cati under moistconditions. The parasite eggs are generallyfound in soil of tropical and sub-tropical coun-tries (Bethony et al. 2006). These parasites maylead to anaemia and growth retardation.

1.5.1 Prevention and Control

• Periodic deworming with anthelmintic drugs.• To generate awareness regarding soil-

transmitted helminths in school children.• Improved personal hygiene.• Control of disease in animal hosts.

1.6 Vector-Borne ParasiticZoonoses

Vector-borne parasitic zoonoses (VBPZ) are thediseases in which zoonotic parasites are trans-mitted from an infected animal to human beingsby an arthropod or other vector. Climate changeand global warming could affect occurrence,intensity and seasonality of many vector-bornezoonotic parasites. VBPZ are important as theyaffect human and animal health (WHO 2004)and cause economic losses (Bram et al. 2001).Factors responsible for emergence of VBPZinclude climate change (Lindgren and Gustaf-son 2001; Rosenthal 2009), increased tourism,animal transport and international food trade(Weijden et al. 2007), drug resistance in parasiteand vector (Takken and Knols 2007), and chan-ges in land-use pattern (Colwell et al. 2011).

VBPZ can be classified either on the basis ofvector involved or into protozoa, cestode andnematode vector-borne zoonoses. Under VBPZ,

1.4 Food Borne Parasitic Zoonoses 13

protozoan-related zoonoses are most importantand significant.

Depending upon the vector involved, VBPZcan be classified into fly, mosquito, mites, bugs,flea and tick-borne parasitic zoonoses(Figs. 1.16, 1.17).

1.6.1 Prevention and Control

1. Use of physical barriers such as mosquitonets.

2. Biological control of vector population.3. Destroy or modify vector breeding grounds.4. Use of chemicals and herbal insecticides as

repellant/killer, etc.5. Reduction in the reservoir hosts of infection.6. Personal prevention strategies.

References

Acha PN, Szyfres B (2006) Zoonoses and communicablediseases common to man and animals. Scientific andtechnical publication No. 580. World Health Organi-zation, Geneva

Anh NTL, Madsen H, Dalsgaard A, Phuong NT, ThanhDTH, Murrell KD (2010) Poultry as reservoir hostsfor fishborne zoonotic trematodes in Vietnamese fishfarms. Vet Parasitol 169:391–394

Ashford RW, Crewe W (1998) The parasites of Homosapiens. Liverpool School of Tropical Medicine,Liverpool

Bethony JR, Brooker S, Albonico M, Geiger SM, LoukasA, Diemert D, Hotez PZ (2006) Soil-transmittedhelminth infections: ascariasis, trichuriasis, and hook-worm. Lancet 367:1521–1532

Bhatia BB (1991) Current status of food-borne parasiticzoonoses in India. In: Cross JH (ed) Emergingproblems in food-borne parasitic zoonosis: impact onagriculture and public health. Proceedings of the 33rdSEAMEO-TROPMED regional seminar. SoutheastAsian J Trop Med Public Health 22:36–41

Bram RA, George JE, Reichard RE, Tabachnick WJ(2001) Threat of foreign arthropod borne pathogens tolivestock in the United States. J Med Entomol39:405–416

Chai JY, Murell KD, Lymbery AJ (2005) Fish-borneparasitic zoonoses: status and issues. Int J Parasitol35:1233–1254

Colwell DD, Torres FD, Otranto D (2011) Vectorborneparasitic zoonoses: emerging scenarios and newperspectives. Vet Parasitol 182:14–21

Cox FEG (2002) History of human parasitology. ClinMicrobiol Rev 15(4):595–612. doi:10.1002/9780470688618.taw0166

Dorny P, Praet N, Deckers N, Gabriel S (2009) Emergingfood-borne parasites. Vet Parasitol 163:196–206

Gajadhar AA, Allen JR (2004) Factors contributing to thepublic health and economic importance of waterbornezoonotic parasites. Vet Parasitol 126:3–14

Gajadhar AA, Scandrett WB, Forbes LB (2006) Over-view of food and water borne zoonotic parasites atthe farm level. Rev Sci Tech Off Int Epiz25(2):595–606

Gracey JF, Collins DS (1992) Meat hygiene (9th edn).Published by Bailliere Tindall educational lowpriced book scheme funded by the Britishgovernment

Lindgren E, Gustafson R (2001) Tickborne encepha-litis in Sweden and climate change. Lancet358:16–18

Parija SC (1990) Review of parasitic zoonoses. AITBSPublishers Distributors, New Delhi

Rosenthal J (2009) Climate change and the geographicdistribution of infectious diseases. EcoHealth6:489–495

Schwabe CW (1984) Veterinary Medicine and HumanHealth, 3rd edn. Williams and Wilkins, USA 428 EastPreston Street

Singh BB, Sharma R, Sharma JK, Juyal PD (2010)Parasitic zoonoses in India: an overview. Rev SciTech Off Int Epiz 29(3):629–637

Singh BB, Sharma R, Gill JPS, Aulakh RS, Banga HS(2011) Climate change, zoonoses and India. Rev SciTech Off Int Epiz 30(3):779–788

Slifko TR, Smith VH, Rose JB (2000) Emerging parasitezoonoses associated with water and food. Int JParasitol 30:379–393

Takken W, Knols BGJ (2007) Emerging pests and vectorborne diseases in Europe. Wageningen AcademicPublishers, Wageningen

van der Weijden WJ, Marcelis RAL, Reinhold W (2007)Invasions of vectorborne diseases driven by transporta-tion and climate change. In:Takken W, Knols BGJ (eds)Emerging pests and vectorborne diseases in Europe.Wageningen Academic Publishers, Wageningen

WHO (1995) Control of foodborne trematode infections.WHO Tech Rep 849:1–157

WHO (2002) Foodborne diseases, emerging.http://www.who.int/mediacentre/factsheets/fs124/en/print.html

WHO (2004) Changing history. World Health Organiza-tion, Geneva

Zhou P, Chen N, Zhang RL, Lin RQ, Zhu XQ (2008)Food-borne parasitic zoonoses in China: perspectivefor control. Trends Parasitol 24(4):190–196

14 1 Introduction

2Protozoonoses

Abstract

Protozoan zoonoses could be defined as ‘‘those protozoan diseases whichare naturally transmitted between (other) vertebrate animals and man’’.Diseases such as toxoplasmosis and cryptosporidiosis are worldwide inoccurrence. Toxoplasma gondii, Cryptosporidium parvum and Sarcocys-tis suihominis are the most significant coccidian parasites affectinganimals and man. Immunocompromised persons are always at higher riskof being infected with zoonotic parasites such as C. parvum, T. gondii,etc. Cryptosporidiosis is an emerging water-borne protozoan disease ofpublic health significance. The parasite Sarcocystis suihominis isprevalent in pigs in Asian countries such as India and China. Africantrypanosomiasis, Chagas disease, leishmaniasis and zoonotic babesiosisare the important vector borne protozoan zoonotic diseases. Africantrypanosomiasis is still a priority zoonosis for the people in sub-SaharanAfrica. The wild rodent P. leucopus acts as an important reservoir forB. microti human infections. Chagas disease is an important medical andeconomic concern in Latin America. Leishmaniasis has been reportedfrom more than 80 countries.

2.1 African Trypanosomiasis

Order: KinestoplastoridaFamily: Trypanosomatidae

2.1.1 Common Name/Synonyms

Nagana (meaning powerless/useless) disease(Winkle 2005) is the common name for thedisease in animals (African animal trypanoso-miasis) and sleeping sickness is the common

name for the disease in humans (human Africantrypanosomiasis).

2.1.2 History

The parasite is present and infecting the people insub-Saharan Africa since many centuries in thepast (Steverding 2008; Cox 2004). T. brucei wasfirst discovered by David Bruce (1855–1931,Scottish microbiologist and pathologist) as thecause of cattle trypanosomiasis (cattle nagana) in1895 (Bruce 1895). After 6 years, trypanosomeswere observed in the human blood for the first

B. B. S. Dhaliwal and P. D. Juyal, Parasitic Zoonoses,DOI: 10.1007/978-81-322-1551-6_2, � Springer India 2013

15

time in 1901 (Forde 1902). The parasite specieswere later identified and proposed as Trypano-soma gambiense (now T. b. gambiense) (Dutton1902). The second trypanosome species patho-genic to human beings, T. rhodesiense (nowT. b. rhodesiense), was later recovered in 1910(Stephens and Fantham 1910).

2.1.3 Epidemiology

The disease is particularly endemic in Africa.Human epidemics due to severe sleeping sick-ness occurred in Africa in the twentieth century(Steverding 2008). T. brucei gambiense is pres-ent in central and western Africa and T. bruceirhodesiense is present in eastern Africa.

2.1.4 Etiology

Two subspecies of T. brucei, T. brucei rhodes-iense and T. brucei gambiense (Bales 1991;Acha and Szyfres 2006) are responsible forhuman African trypanosomiasis (sleeping sick-ness). T. brucei brucei, the third subspecies onlycauses infection in animals. The chronic andepidemic form of sleeping sickness generallyoccurs due to T. b. gambiense, whereasT. b. rhodesiense infection is responsible for theacute form of the disease.

2.1.5 Reservoir

Human beings act as important reservoirs ofT. b. gambiense. Wild and domestic animalscould also act as important parasite reservoirs forhuman trypanosomiasis (WHO 2006; Njiokouet al. 2006; Simo et al. 2006; Steverding 2008).

2.1.6 Transmission

The bite of an infected tsetse fly belonging togenus Glossina transmits the infection from onehost to the other (Fig. 2.1).

2.1.7 Clinical Signs in Man

The bite of an infected fly leads to eruption ofred sores at the region of the bite. Symptomssuch as fever, swollen lymph glands, headachesand irritability and aching muscles and joints,could arrive within a few weeks.

The disease progresses through two distinctstages. During the initial stage or haemolymphaticphase, the parasite infects the blood and lymphsystem (WHO 2006). The corresponding symp-toms include fever, headache, joint pain and itch-ing. In the later stages (neurological phase), theinvolvement of nervous system leads to symptomssuch as changes in personality, alteration of thebiological clock (the circadian rhythm), confusion,slurred speech, seizures and difficulty in walkingand talking (WHO 2006). This is generally char-acterised by the presence of trypanosomes in thecerebrospinal fluid (WHO 2006). Death may occurin untreated patients within months (in case ofT. b. rhodesiense infections) or within years(in case of T. b. gambiense infections) dependingupon the species involved.

2.1.8 Clinical Signs in Animals

Infections due to T. b. rhodesiense are gener-ally asymptomatic in domestic (cattle andsheep), wild and laboratory animals (Acha andSzyfres 2006). The second parasite species,T. b. gambiense has been occasionally isolatedfrom laboratory animals with no evidence thatit causes disease (Acha and Szyfres 2006).

2.1.9 Diagnosis

The disease may be diagnosed from clinicalsigns; demonstration of the parasite from lymphgland and cerebrospinal fluids, bone marrow andblood; mice inoculation and culture in specialmedia such as glucose, lactoalbumin or GLSH.Serological tests such as card agglutination,ELISA, indirect hemagglutination may also beused but they are of limited value.

16 2 Protozoonoses

2.1.10 Control

The control of the disease includes reduction inthe reservoir host and vector population, che-motherapy and chemoprophylaxis.

2.2 Amoebiasis

Subphylum: SarcodinaOrder: AmoebidoridaFamily: Endamoebidae

2.2.1 Common Name/Synonyms

The disease is known as amoebiasis, amoebicdysentery and entamoebiasis.

2.2.2 History

The amoebae were first found in faecal samples byFeder Losch in 1875 in Saint Petersburg, but he didnot regard them as a cause for dysentery (Pinillaet al. 2008). Later, E. histolytica were pointed out

to be a species complex by Emile Brumpt in 1925,comprising two morphologically similar species,E. dysenteríae and E. dispar found in symptomaticand asymptomatic carriers, respectively (Pinillaet al. 2008). In 1993, Diamond and Clark alsoagreed to Brumpt’s original 1925 hypothesis, withsimilar conclusions (Pinilla et al. 2008). Thishypothesis was accepted by the World HealthOrganisation in 1997 (Pinilla et al. 2008).

2.2.3 Etiology

E. histolytica and E. polecki are of zoonoticimportance. Knowledge regarding E. dispar isquite limited. Most of the asymptomatic amoe-bic infections occur due to E. dispar, althoughE. histolytica asymptomatic colonisation is alsonot uncommon (Braga et al. 1996; Haque et al.1997; Cantellano and Palomo 2000).

2.2.4 Epidemiology

Amoebiasis due to Entamoeba histolytica has aworldwide distribution (WHO 1969, WHO 1985).

Fig. 2.1 Life cycle of T.b. rhodesience

2.1 African Trypanosomiasis 17

Most of the infections have been reported in thedeveloping countries of Central and SouthAmerica, Africa and Asia.

2.2.5 Reservoir

Man is an important reservoir of E. histolytica.

2.2.6 Transmission

Food and water contaminated with faecal matterserve as important sources of infection. Addi-tionally, flies could act as vectors and carry thecysts (Acha and Szyfres 2006).

2.2.7 Life Cycle

The life cycle involves trophozoites which arepresent in host’s large intestine and cysts whichare shed in the faeces of the host. Humansbecome infected by ingesting cysts, throughcontaminated food or water.

2.2.8 Clinical Signs in Man

According to WHO, 50 million cases of colitisand liver abscess and 100,000 deaths resultannually from infection by this organism (WHO1995).

In most cases, the infection remains asymp-tomatic as the parasite lives in the intestine anddoes not cause disease, or causes mild disease.Symptoms of this form include loose or waterystools, abdominal discomfort and stomachcramps. Sometimes, a severe form amoebicdysentery could develop leading to stomachpain, bloody stools and fever. In rare cases, theparasite reaches the liver and forms abscesses.

2.2.9 Clinical Signs in Animals

The disease due to E. histolytica could occur innon-human primates. The parasite has also been

reported from dogs, rats, cats, swine and cattle(Levine 1985). E. polecki has been commonlyreported in swine (Pakandl 1994).

2.2.10 Diagnosis

The disease may be diagnosed from directdemonstration of the parasite (trophozoites andcysts) from faeces, or using specific trichrome oriron hematoxylin staining techniques (Fotedaret al. 2007). The advanced diagnostic testsinclude identification of the parasite based ondetection of E. histolytica-specific antigen andDNA in stool and other clinical samples.Molecular diagnostic tests, such as conventionaland real-time PCR, have also been developed forthe detection and differentiation of E. histolyticaand E. dispar in recent years.

2.2.11 Control

The control of the disease includes improvedpersonal hygiene and avoiding contamination offood and water with infected faeces.

2.3 Babesiosis

Class: PiroplasmidaFamily: Babesiidae

2.3.1 Common Name/Synonyms

The disease is known as babesiasis, piroplas-mosis.

2.3.2 History

Babesia divergens was first described and namedPiroplasma divergens in 1911 (M’Fadyean andStockman 1911). Later, the parasite B. divergenswas identified as the causative agent of the dis-ease in splenectomised humans (Fitzpatrick et al.1968).

18 2 Protozoonoses

The first human case was reported fromCroatia (then Yugoslavia) in 1956. B. divergens(cattle parasite) was believed to be the cause forthis infection. This parasite is mainly responsi-ble for zoonotic babesiosis in Europe (Zintl et al.2003). Another authenticated case due toB. microti has also been recorded from Europe(Hildebrandt et al. 2007).

2.3.3 Etiology

B. microti (Gorenflot et al. 1998; Homer et al.2000; Kjemtrup and Conrad 2000; Telford et al.1993; Telford and Spielman 1997) andB. divergens (Beattie et al. 2002; Herwaldt et al.1996; Olmeda et al. 1997) are the two importantspecies responsible for zoonotic babesiosis.

2.3.4 Epidemiology

In Europe, most cases of human babesiosis arecaused by Babesia divergens (Genchi 2007).Epidemiological surveys have revealed the pres-ence of B. divergens throughout Europe and mayextend beyond Europe into North Africa (Zintlet al. 2003). Human babesiosis due to B. microtiwas reported in the USA in 1969 (Westernet al. 1970). Thirty-one human cases of Babesiainfections have been reported from splenecto-mised individuals in Europe (Gorenflot et al.1998; Marsaudon et al. 1995; Hunfeld et al. 2002).

2.3.5 Reservoir

Infected rodents and animals can serve asimportant reservoirs for other animals. The wildrodent P. leucopus acts as an important reservoirfor B. microti human infections.

2.3.6 Transmission

Ixodes ricinus transmits Babesia divergens andI. scapularis transmits B. microti (Hunfeld andBrade 2004). The adult I. ricinus female

acquires the infection from the infected host andcan transmit transovarially to larvae (Beckeret al. 2009; Zintl et al. 2003) (Fig. 2.2).

2.3.7 Clinical Signs in Man

In immunocompromised patients, acute illnessdue to B. divergens appears suddenly, with hae-moglobinuria as important symptom (Telfordet al. 1993). Persistent high fever (40–41 �C),chills, intense sweats, headaches, myalgia andlumbar and abdominal pain are the other impor-tant symptoms. Vomiting and diarrhoea may alsooccur in a few cases (Gorenflot et al. 1998).Haemolysis could lead to jaundice (Hunfeld et al.2008). Anoxia and toxic waste products couldresult in further complications such as respira-tory, cardiac, renal or hepatic failure.

B. microti might result in acute and mildinfections in immunocompromised and immu-nocompetent individuals, respectively. Asymp-tomatic infections are also not uncommon. Thereported case of an immunocompromised indi-vidual showing symptoms such as fever andchest pain was successfully treated (Hildebrandtet al. 2007). In immunocompromised humans,this parasite may cause medical emergencies dueto rapid fulmination and parasitemias that mayexceed 70 % (Zintl et al. 2003).

2.3.8 Clinical Signs in Animals

In severe cases, there may be fever, anaemia,anorexia, depression and increased respiratoryand heart rate. The mucous membranes becomepale and may be jaundiced (Christensson 1989;Collins et al. 1970; Gray and Murphy 1985;Sherlock et al. 2000). Erythrocyte destructionleads to haemoglobinuria. Death generallyoccurs due to cardiac failure, hepatic or renalinsufficiency (Collins et al. 1970).

2.3.9 Diagnosis

The preliminary diagnosis can be done fromclinical signs such as high fever with

2.3 Babesiosis 19

haemoglobinuria. Definitive diagnosis can bedone with the detection of the parasite in theerythrocytes. Single round or oval forms aregenerally seen in both species. Advanced diag-nostics include serological tests such as IFATand PCR analysis followed by sequencing of thePCR product. Inoculation of infected materialinto splenectomised calves or gerbils is anothersensitive method for detection of the parasite(Gray et al. 1989; Joyner and Davies 1967;L’Hostis et al. 1995).

For detecting B. divergens in ticks, micro-scopic examination of Giemsa-stained smears ofgut or other tick tissues (Gern and Brossard1986; Koch 1906), xenodiagnosis and PCR (Duhet al. 2001) are of great diagnostic value.

2.3.10 Control

Avoid contact with ticks as the infection occursthrough tick bites. Asplenic and immunocom-promised individuals are at the greatest risk and

should take extra care particularly when visitingendemic areas.

2.4 Balantidiosis

Phylum: CiliophoraOrder: TrichostomatoridaFamily: Balantidiidae

2.4.1 Common Name/Synonyms

Balantidiosis is also known as balantidiasis,balantidial or ciliary dysentery.

2.4.2 Etiology

The disease occurs due to Balantidium coli. It isthe largest ciliate protozoan and can infectswine, primates, man and rarely rats, guinea pigsand dogs.

Fig. 2.2 Life cycle of B. microti /B. divergens

20 2 Protozoonoses

2.4.3 History

Malmsten reported B. coli from two patientswith severe diarrhoea in 1857 (Kean et al. 1978).

2.4.4 Epidemiology

The disease is endemic and prevalent world-wide, mostly prevalent in temperate and tropicalregions (Arean and Koppisch 1956). B. coli canbe found in many primates (Nakauchi 1999).

2.4.5 Transmission

Pigs and rat are important sources of infectionfor human beings (Esteban et al. 1998). Man-to-man transmission could occur due to poor per-sonal/environmental hygiene (Giacometti et al.1997). Non-human primates could also transmitthe infection. Humans generally act as asymp-tomatic carriers of B. coli (Esteban et al. 1998).Contaminated water or food containing cystsserve as an important source of infection forhuman beings.

2.4.6 Life Cycle

The cysts shed in the faeces by infected hostscause infection in the susceptible host throughfaecal oral route after ingestion of cyst con-taminated water or food.

2.4.7 Clinical Signs in Man

Balantidiosis at times may resemble intestinalamoebiasis. The acute form is recognised byrapid onset of diarrhoea or dysentery (Castroet al. 1983) and other signs like abdominal colic,nausea and vomiting. In the chronic form, thereare episodes of intermittent diarrhoea alternatingwith normal bowel movements or constipation.Other signs like headache, anorexia, weight lossor muscular weakness could also be present.

2.4.8 Clinical Signs in Animals

The parasite is generally non-pathogenic or cau-ses asymptomatic disease in swine or primates.

2.4.9 Diagnosis

The disease may be diagnosed from direct dem-onstration of the parasite (trophozoites and cysts)from faeces or intestinal scrapings, in wet mountsof fresh faeces. Trophozoites are usually presentin diarrhoeic stools and cysts in solid stools.

2.4.10 Control

The control of the disease includes avoidingcontamination of food and water with infectedfaeces and treatment of infected cases

2.5 Chagas Disease

Order: KinestoplastoridaFamily: Trypanosomatidae

2.5.1 Common Name/Synonyms

The disease is also known as American try-panosomiasis or Chagas mazza disease.

2.5.2 Etiology

American trypanosomiasis/chagas disease iscaused by the protozoan Trypanosoma cruzi.The parasite multiplication generally occursinside the heart and smooth muscle cells.

2.5.3 Epidemiology

Chagas disease is an important medical andeconomic concern in Latin America (Miles et al.2003). According to a survey, more than 10

2.4 Balantidiosis 21

million people act as carriers of Trypanosomacruzi (Collier et al. 1997).

2.5.4 Transmission

Many species of triatomine bug are known(Carcavallo et al. 1998) to carry T. cruzi. Theparasite is transmitted by many species of triato-mine bugs, due to deposition of faeces by infectedvector on the mucous membranes or abraded skin(Miles et al. 2003). Triatomine bugs do not fly tohosts to take a blood meal as in the case of tsetsefly vectors of African trypanosomiasis (Fig. 2.3).The infection occurs when some species oftriatomine bugs colonise houses in large numbersleading to feeding from humans, domestic mam-mals and chickens. The chickens are not suscep-tible to infection, but could serve as an importantsource of blood meal (Miles et al. 2003).

2.5.5 Reservoir

Infected mammals such as armadillo, carnivo-rous animals (dog and cat) and rodents couldserve as reservoirs of infection.

2.5.6 Clinical Signs in Man

Chagas disease is an important cause for heartdisease in Latin America (Tanowitz et al. 1992,Amorin 1979). As per estimates, approximately50,000 deaths have been found associated withthe infection (Espinosa et al. 1985, Garcia-Zapata and Marsden 1986).

2.5.6.1 Acute Clinical Chagas DiseaseThe disease may remain asymptomatic or pres-ent clinical signs. Inflammatory lesion which isalso known as a chagoma may develop at thesite of entry of the T. cruzi (Tanowitz et al.1992). It is generally followed by fever, myal-gia, cephalalgia and unilateral eyelid swelling(Acha and Szyfres 2006).

2.5.6.2 Chronic ChagasCardiomyopathy

Chronic chagas disease may lead to symptomssuch as arrhythmias, thromboembolic events(Oliveira et al. 1983) or congestive heart failure(Tanowitz et al. 1992).

2.5.7 Clinical Signs in Animals

The disease is generally asymptomatic amongwild animals. Symptoms such as fever, palpebraledema, hepatomegaly and alterations in nervoussystem could occur in dogs (Acha and Szyfres2006).

2.5.8 Diagnosis

The disease may be diagnosed from clinicalsigns, demonstration of the parasite from blood,serological testing, laboratory animal inocula-tions and molecular techniques such as PCR.

2.5.9 Control

Combined international efforts have led to sig-nificant reductions in the adverse impact ofchagas disease in the recent years in the Amer-icas (Dias et al. 2002). Use of pesticides such asorganochlorines (dieldrin and gamma-BHC) andother synthetic pyrethroids have effectivelycontrolled vector populations (Dias et al. 2002).Successful implementation of control measuresfor chronic chagas disease have led to themoving of age-specific mortality from the clas-sical 35–55 years to age groups higher than60 years (Dias 2000).

2.6 Cryptosporidiosis

Subclass: CoccideaFamily: Cryptosporidiidae

22 2 Protozoonoses

2.6.1 Common Name/Synonyms

The disease is also known as Cryptosporidiuminfection.

2.6.2 History

Cryptosporidium is recognised as an importanthuman parasite since 1976 (Current and Garcia1991, Fraser et al. 1997). C. parvum has beenresponsible for several water-borne outbreaks(Hayes et al. 1989, MacKenzie et al. 1994).Since 1982, cryptosporidiosis has been increas-ingly recognised as a cause for severe and life-threatening diarrhoea in AIDS patients (Current1983).

2.6.3 Epidemiology

Cryptosporidiosis is an emerging water-borneprotozoan disease of public health significanceworldwide. Cryptosporidium parvum has theability to cause gastrointestinal illness in a widevariety of mammals, including humans, cattle,sheep, goat, pig and horses across the globe(Fayer 1997). C. parvum has been associatedwith neonatal calf diarrhoea (Nydam et al. 2001;Singh et al. 2006) and 1- to 3-week-old calvesare most susceptible (Leek and Fayer 1984;Singh et al. 2006). The parasite has also beenreported in cattle over 2 years of age (Henriksenand Krogh 1985). C. parvum is identified as acommon cause for diarrhoea in immunocompe-tent individuals. In immunodeficient individuals,

Fig. 2.3 Life cycle of T. cruzi

2.6 Cryptosporidiosis 23

the parasite may lead to life-threatening chronicdiarrhoea. In Acquired Immuno DeficiencySyndrome (AIDS) endemic areas in the devel-oping world, the parasite poses a significantpublic health problem (Casemore and Wright1997; Griffiths 1998; O’Donoghue 1995).Infection rates are predicted to be highest indeveloping countries and in children (Fayer1997).

2.6.4 Transmission

The disease occurs through the faecal oral routewhen oocysts excreted by infected man/animalscontaminate food and water. The contaminatedfood and water when ingested leads to infectionin other susceptible hosts.

2.6.5 Reservoir

Neonatal calves are an important source ofinfection to man.

2.6.6 Clinical Signs in Animals

The disease in calves is characterised by weightloss and watery diarrhoea. But it is necessary todistinguish the infection from many other causesof calf diarrhoea. Calves 7- to 21-days old seemto be most susceptible to this infection (Aiello1998; OIE 2005).

2.6.7 Clinical Signs in Man

Clinical signs mainly include watery diarrhoea,stomach cramps and slight fever. Immunocompromised individuals are not able to clearthe parasite (Angus 1983). In immunodeficienthuman beings, Cryptosporidium could lead tolife-threatening chronic diarrhoea.

2.6.8 Diagnosis

The disease can be diagnosed by identifying theoocyst stage of the parasite in host faeces (Garciaet al. 1983; Casemore et al. 1985) or in histo-logical sections taken during necropsy (Current1985). Detection of the parasite in the faeces canbe done by using acid fast or immunofluores-cence staining of unconcentrated faecal smears.Appropriate concentration methods could beused when small numbers of oocysts are present.The parasite can be detected in mucosal scrap-ings of fresh intestine. Concentration techniquessuch as faecal flotation in sucrose or zinc sul-phate solutions could be used. Polymerase chainreaction (PCR) could be used to detect crypto-sporidiosis in water supplies or asymptomaticcarriers. The World Organisation for AnimalHealth (OIE) recommends modified Ziehl-Neelson (mZn) acid fast staining and sheather’ssucrose floatation method for detection ofoocysts from faeces (OIE 2005) (Figs. 2.4, 2.5).

2.6.9 Control

Prevention and control measures include use ofboiled, filtered or bottled water. Maintain goodpersonal hygiene and wash hands thoroughlyafter any contact with stools. Persons withweakened immune system must take extraprecautions.

2.7 Giardiosis

Class: ZoomastigophoraOrder: DiplomonadidaFamily: Diplomonadida

2.7.1 Common Name/Synonyms

Giardia enteritis

24 2 Protozoonoses

2.7.2 Etiological Agent

Giardia intestinalis (syn. duodenalis or lamblia)is a water-borne pathogen and can infect allmammals. The presence of zoonotic genotypes(assemblages A and B) in animals such as dogsand cattle is of public health significance(Hamnes et al. 2006). Cattle are susceptible toinfection with three genotypes of G. intestinalis,the zoonotic genotypes of assemblages A and B(Lalle et al. 2005) and the hoofed livestockgenotype of assemblage E (Thompson 2004).

2.7.3 Epidemiology

The intestinal flagellate Giardia intestinalis isglobally distributed and commonly infects manyanimal species and man (Xiao 1994; Kulda andNohykova 1995). Giardiosis is worldwide andoccurs in both developed and developing coun-tries (Fraser et al. 1997; Gilman et al. 1988;Islam et al. 1983; Addiss et al. 1991; Rauch et al.1990; White et al. 1989; Birkhead and Vogt1989; Singh et al. 2008).

2.7.4 Reservoir

Humans act as the main reservoir of infection forhumans. The parasite is prevalent in bovinepopulations (Buret et al. 1990; Iburg et al. 1996;Olson et al. 1997) which could serve as a sourceof contamination to water supplies as Giardiacyst travels through the environment (Barwicket al. 2003). It has been suggested that the fewoutbreaks in humans might have resulted due tocontamination of drinking water by dairy pasturerunoff (Degerli et al. 2005). There is evidencesuggesting it to be a zoonosis (Buret et al. 1990).Thus farmers, veterinarians and techniciansworking in close contact with infected animalsmay be at risk of contacting the disease. Sinceinfected calves excrete high numbers of Giardiacysts, they are considered to be the mostimportant source of contamination for theirspecies (Xiao and Herd 1994; Xiao et al. 1993).Although Giardia is more prevalent in calves,adult animals serve as reservoirs of infection(McAllister et al. 2005).

2.7.5 Transmission

Infection takes place through faecal oral route.Cysts of G intestinalis, shed by faeces, areingested orally via water, milk and feed (Gozet al. 2006).

Fig. 2.4 Cryptosporidium oocysts from a Sheather’sfloation of faecal samples (with kind permission from Dr.Alvin A Gajadhar, Research Scientist cum Head, Centrefor Food-Borne and Animal Parasitology, Canadian FoodInspection Agency Saskatoon Lab, Canada)

Fig. 2.5 Cryptosporidium oocysts from modified Ziehl-Neelson’s staining of faecal samples

2.7 Giardiosis 25

2.7.6 Clinical Signs in Man

The disease is generally asymptomatic or sub-clinical (Farthing 1996). The important symp-toms include diarrhoea, bloating and abdominalpain. Recurring diarrhoea and flatulence mightpersist in some patients.

2.7.7 Clinical Signs in Animals

The severity of G. intestinalis infections variesfrom asymptomatic to clinical disease (Xiaoet al. 1993; Quilez et al. 1996). The symptoms incalves include mucoid and fatty stool, weightloss and growth retardation (Dwight 1999; Xiaoand Herd 1994). An infected animal shedsmicroscopic cysts with the faeces and intermit-tent cyst shedding can continue for severalweeks in calves (Xiao and Herd 1994).

2.7.8 Diagnosis

Faecal samples can be examined by wet mount(native lugol) and Wheatley’s trichrome (Modifi-cation of Gomori Trichrome) staining technique(Garcia 2001; Wheatley 1951). If the number ofoocysts in faecal material is fairly low or absent,then sucrose floatation should be followed bystaining techniques. For trichrome staining, mod-erately thick faecal smears should be prepared andimmediately fixed in Schaudinn’s fixative for aminimum of 30 min. Microscopic examinationshould be done at magnification(s) of 40X and100X. Morphometric studies of Giardia cysts andtrophozoites can also be carried out (Fig. 2.6).

2.7.9 Prevention and Control

Avoid contamination of drinking water withfaecal matter.

2.8 Leishmaniasis

Class: ZoomastigophoraFamily: TrypanosomatidaeGenus: Leishmania

Leishmaniasis is a complex group of diseasesendemic in many parts of the world. Leish-maniasis could occur due to more than 20Leishmania species. The parasite is transmittedto human beings by many species of phleboto-mine sand flies (Chappuis et al. 2007; Herwaldt1999; Pearson and Sousa 1996).

Leishmaniasis has been reported from 88countries. Ninety percent of visceral leishmani-asis cases have been reported from five coun-tries: India, Bangladesh, Nepal, Sudan andBrazil (NICD 2006). Some workers believeIndian kala-azar to be anthroponotic due toabsence of animal reservoirs.

Leishmaniasis occurs in four clinical forms:Cutaneous leishmaniasis; muco-cutaneousleishmaniasis; visceral leishmaniasis and post-kala-azar dermal leishmaniasis.

Fig. 2.6 Giardia cysts from a zinc sulphate flotation offaecal samples (with kind permission from Dr. Alvin AGajadhar, Research Scientist cum Head, Centre for Food-Borne and Animal Parasitology, Canadian Food Inspec-tion Agency Saskatoon Lab, Canada)

26 2 Protozoonoses

2.8.1 Visceral Leishmaniasis

2.8.1.1 Common Name/SynonymsBlack fever, Kala-azar, dumdum fever, post-kala-azar dermal leishmaniasis.

2.8.1.2 EtiologyThe disease occurs due to Leishmania donovanicomplex—L. donovani sensu stricto in Indiansubcontinent, East Africa and the L. infantum inNorth Africa, Europe and Latin America (Lukes2007; Chappuis et al. 2007; Mauricio et al.2000). The disease occurs due to L. chagasi inthe American continent. L. donovani causes an-throponotic, whereas L. infantum is responsiblefor zoonotic visceral leishmaniasis. The diseasecould become fatal if not properly treated.

2.8.1.3 ReservoirDogs principally act as reservoir hosts for spreadof zoonotic visceral leishmaniosis (VL) whichmainly occurs due to transmission of L. Infantum(Chappuis et al. 2007; Alvar et al. 2004).

2.8.1.4 TransmissionThe transmission of the parasite occurs due tobite of sand flies belonging to either Phleboto-mus or Lutzomyia spp.

2.8.1.5 EpidemiologyThe parasite L. infantum mostly infects childrenand immunosuppressed individuals, whereasL. donovani could infect all age groups(Chappuis et al. 2007). Estimated 500,000 newcases and more than 50,000 deaths occur due tovisceral leishmaniasis every year (Chappuiset al. 2007; Desjeux 2004a, b).

From a total of approximately 500,000 vis-ceral leishmaniasis cases occurring annuallyacross the globe, more than 23,000 cases arereported from India. The present foci of thedisease in India are Bihar, West Bengal, Uttar

Pradesh and Jharkhand (Sutherst 1993). Spo-radic cases have also been reported from Gujarat(west India) (Munshi et al. 1972), Tamil Naduand Kerala (south India) and sub-Himalayanparts of north India including Uttar Pradesh,Himachal Pradesh and Jammu and Kashmir(Kesavan et al. 2003). It was a common beliefthat western India has become a VL free zone,but recent studies (Sharma et al. 2007) havereported that the population of Gujarat state isagain at risk of kala-azar after about 20 years.

The disease is a serious problem in Bihar,West Bengal and eastern Uttar Pradesh states ofIndia where there is under-reporting of kala-azarand post-kala-azar dermal leishmaniasis inwomen and children 0–9 years of age (Bora1999). The parasite and the disease were firstreported in India in the 1820s in undividedBengal. The disease almost disappeared in the1950s but resurgence was reported in the 1970sin north Bihar (NICD 2006). Recent outbreaksof VL in India and the epidemic of humanimmunodeficiency virus (HIV) makes VL are-emerging problem in India. Outbreaks andepidemics have been associated with climatechange, urban development, deforestation andhuman migration. The prevalence of HIV sero-positivity in VL patients was found to be 5.7 %(6/104) at a tertiary care centre in northern India(Mathur et al. 2006). Four of the six (67 %)VL/HIV co-infected patients had a chronic/relapsing course, not responding to antileish-manial treatment.

The first indigenous case of visceral leish-maniasis in a 7-year-old girl from central India(Dey et al. 2007) indicated that more than onegenetic variant of L. donovani is circulating indifferent parts of India. The co-existence ofmalaria and kala-azar poses difficulties in dif-ferential diagnosis and results in lower reportingof the disease. Examination of Leishmania-stained blood smears of 450 asymptomatichealthy individuals residing in an endemic vil-lage in Bihar (Sharma et al. 2000), showed thepresence of Leishmania amastigotes in six per-sons (1.3 %).

2.8 Leishmaniasis 27

2.8.1.6 Clinical Signs in ManThe incubation period of the disease is between2 and 6 months. The symptoms mainly resultdue to systemic infections. Symptoms includeloss of appetite, fever, fatigue, weakness andweight loss. Due to invasion of the parasite inthe blood and reticuloendothelial system,enlargement of lymph nodes, spleen and livercould occur. The feet, hands, abdomen and skinmay take a grey hue particularly in Indianpatients.

2.8.1.7 Clinical Signs in AnimalsThe disease can occur in dogs and could causecutaneous or systemic lesions. Cutaneoussymptoms include alopecia and inflammationleading to formation of nodules, scabs andulcers. Systemic symptoms include fever, anae-mia, splenomegaly and lymphadenopathy.

2.8.1.8 Diagnosis• Microscopic examination of blood, lymph

nodes, bone marrow or spleen aspirates for theidentification of amastigote form of theparasite.

• Serological tests.• Molecular techniques such as Polymerase

chain reaction.

2.8.1.9 ControlThe control measures for visceral leishmaniasisinclude control of the disease in reservoir andvector, use of insecticide impregnated materialsand active detection and treatment of cases(Chappuis et al. 2007; Boelaert 2000; Davieset al. 2003).

2.8.2 Cutaneous Leishmaniasis

2.8.2.1 Common Name/SynonymsDelhi sore, Oriental sore, Baghdad ulcer, Uta,Buba.

2.8.2.2 EtiologyCutaneous Leishmaniasis can occur due to manyLeishmania species and sand flies transmit theinfection to human beings and animals(Reithinger et al. 2007). Most Leishmania spe-cies could cause cutaneous leishmaniasis inhuman beings.

L. braziliensis complex, L. mexicana com-plex, L. lainsoni, L. naiffi and L. lindenbergicause the disease in the new world. L. tropicacomplex (L. tropica, L. major and L. aethiopica)species cause the disease in old world. Somestrains of L. infantum can also cause cutaneousleishmaniasis. With the exception of L. tropica,all the other organisms are zoonotic in nature.

2.8.2.3 EpidemiologyCutaneous leishmaniasis endemic in the tropicsand neotropics (Reithinger et al. 2007). Cuta-neous leishmaniasis is endemic in more than70 countries worldwide. Ninety percent of casesoccur in countries such as Afghanistan, Pakistan,Saudi Arabia, Algeria, Brazil, Peru and Syria(Desjeux 2004a, b). The disease is spreading tonew areas as a result of urbanisation and defor-estation (Desjeux 2001). In India, initially thedisease was reported from hot dry northwesternregion and was endemic in western Thar desertof Rajasthan (NICD 2006). Sporadic cases werealso reported from Punjab, Delhi, Haryana andGujarat (Shahi 1941; Lysenko 1971). New fociof infection have been reported from differentparts of India (Bora et al. 1996; Sharma et al.2003). Kerala remained free from cutaneousleishmaniasis (CL) since 1988, many cases havebeen recorded afterwards (Bora et al. 1996;Kumaresan and Kumar 2007). This is animportant public health issue in view of a newlyrecognised reservoir area of CL in South India.

2.8.2.4 ReservoirMany domestic animals could serve as potentialreservoirs (Davies et al. 2000; Reithinger et al.2003). Both dogs and rodents serve as the zoo-notic reservoirs for cutaneous leishmaniasis in

28 2 Protozoonoses

the Thar desert (Ahuja et al. 2006). In dogs, anincidence of 6.8 and 6.12 % was recorded during1985 (Nirban 1985) and 1999 (Chhangani 1993),respectively, in Bikaner. Natural Leishmaniainfections are found in a variety of non-humanmammal hosts (e.g. rodents, edentates, marsu-pials and carnivores). So far, only a fewreservoir hosts for the main Leishmania spp(i.e. L infantum, L amazonensis, L peruviana,L mexicana, L panamensis, L guyanensis,L major and L aethiopica) have been reported(Davies et al. 2000; Ashford 1996).

2.8.2.5 TransmissionThe transmission of the parasite occurs due to thebite of sand flies belonging to either Phlebotomus(in Asia, Europe, North Africa and middle east) orLutzomyia species (from southern USA to north-ern Argentina) (Killick-Kendrick 1999) (Fig. 2.7).

2.8.2.6 Clinical Signs in ManSeveral Leishmania spp. can cause cutaneousleishmaniasis in human beings, although mostinfections generally remain asymptomatic(Murray et al. 2005). Initially, a small erythemadevelops after the bite of an infected sand fly.

The erythema further develops into a papule,then a nodule which ulcerates over a period of2 weeks to 6 months and becomes the lesioncharacteristic of localised cutaneous leishmani-asis (Peters and Killick-Kendrick 1987). In dis-seminated cutaneous leishmaniasis, non-ulcerative nodules disseminate from the initialsite of infection and could cover the entirehuman body (Peters and Killick-Kendrick 1987).Mucosal involvement could also occur inL braziliensis infections and could lead to life-threatening mucosal leishmaniasis in somepatients (Reithinger et al. 2007).

2.8.2.7 Clinical Signs in AnimalsThe disease could occur in dogs which can showboth cutaneous and visceral manifestations(Acha and Szyfres 2006).

2.8.2.8 Diagnosis• Microscopic examination in the lesions for

identification of amastigote form of the parasite.• Isolation of the organism by culture in suitable

media.• Immunological tests.

Fig. 2.7 Life cycle of Leishmania spp. causing cutaneous leishmaniasis

2.8 Leishmaniasis 29

2.8.2.9 ControlThe control measures for cutaneous leishmani-asis include control of infection in reservoir andvector and the use of insecticides.

2.9 Sarcocystosis

Subclass: CoccidiaOrder: EucoccidioridaFamily: Sarcocystidae

2.9.1 Common Name/Synonyms

Sarcosporidiosis

2.9.2 Etiological Agent

Sarcocystosis is a protozoan disease of almostall species of domestic animals caused by Sar-cocystis sp. Cattle and pig act as the mainsources of human disease. Three species ofSarcocystis have been recognised in cattle, ofthese, S. cruzi has the dog as its definitive host,S. hirsuta the cat and S. hominis the man. Pigharbours three species of Sarcocystis namely,S. miescheriana, S. porcifelis, and S. suihominiswith their definitive hosts as dog, cat and man,respectively. Sarcocysts have been commonlyfound in retailed foods and can remain viable forseveral days under refrigeration conditions.

2.9.3 Life Cycle

Human beings act as definitive host for S. homi-nis, S suihominis and get infected by eating rawor undercooked beef and pork, respectively.Meat with visible sarcocysts is unacceptable tothe consumer and the condemnation of carcassesleads to considerable losses to the meat industry.In intermediate hosts, signs are evident at thetime when vascular endothelium is parasitised byschizonts. Later, the schizonts disappear withinabout a month and lead to formation of cysts inthe muscles (Fig. 2.8).

2.9.4 Epidemiology

Previous studies indicate high incidence of sar-cocystosis all over the world (Carvalho 1993,Dubey et al. 1989, Foggin 1980; Shi and Zhao1987; Stalheim et al. 1980; Singh et al. 2003,2004; Avapal et al. 2002, 2004; Juyal et al. 1982;Juyal 1991; Juyal and Bhatia 1989). Studies usingconventional techniques have reported the pres-ence of S. suihominis in India (Banerjee et al.1994; Bhatia 1991). Sarcocystis species has beenreported from many countries. In India, S. cruzihas been reported from Uttranchal, MadhyaPradesh, Bihar and Assam, whereas S. hominishas been reported from Uttar Pradesh andMadhya Pradesh states only (Devi et al. 1998;Jain and Shah 1988; Pandit et al. 1994; Salequeand Bhatia 1991; Singh 2001; 2002). Sarcocystisspecies mainly infect skeletal and cardiacmuscles. Sarcocystis species has been found inthe muscles of oesophagus, thigh, cardiac, dia-phragm, eye, tongue and tail.

2.9.5 Clinical Signs in Animals

The disease is also of economic importance, as itcauses both direct and indirect economic losses.Direct losses arise through losses incurred indetaining or condemning carcasses and indirectlosses arise from delayed growth and productionlosses on the farm. In heavy infections ofintermediate host (cattle), important symptomsinclude anorexia, pyrexia (42 �C or more),anaemia, cachexia, enlarged palpable lymphnodes, excessive salivation, nervousness, lame-ness and hair loss on the extremities.

Hair loss is noticed especially at the end ofthe tail and complete loss of the switch gives theanimals a ‘‘rat tail’’ appearance. The cystic stageof sarcocystosis is virtually non-pathogenic.Pathological changes observed at necropsyinclude eosinophilic myositis (Jensen et al.1986), generalised lymphadenopathy, erosionsand ulcerations in the oral cavity and oesopha-gus and severe laminitis. Histologically, there islymphadenitis, myositis, myocarditis and

30 2 Protozoonoses

glomerulonephritis. Schizonts of Sarcocystisspecies may be found in the endothelial cells ofblood vessels in many organs. Abortions mayoccur in breeding stocks.

2.9.6 Clinical Signs in Man

Human sarcocystosis is reviewed under two sec-tions: Intestinal sarcocystosis, where man acts as adefinitive host and muscular sarcocystosis, whereman acts as an intermediate host for various Sar-cocystis species. Intestinal sarcocystosis is mainlycharacterised by abdominal pain and diarrhoea.The muscular form of the disease is characterisedby pain, swelling, stiffness and displacement ofmyofibrils in the affected muscles.

2.9.7 Diagnosis

Samples of the animal’s muscle tissues like thigh,cardiac, jaw, tail, diaphragm, neck, eye muscles,oesophagus and brain should be collected inpolythene bags containing ice at 4 �C. Theyshould be first examined grossly and then sub-jected to pepsin digestion method (Jacob et al.1960) after removing fat and connective tissue.The diagnosis from muscles can be done using thefollowing methods: (Figs. 2.9, 2.10, 2.11)• Isolation of intact microsarcocysts from

muscles (Juyal et al. 1989).• Pepsin digestion technique.• Histopathological examination (Luna 1968).• Serological tests like ELISA, etc.• Electron microscopic studies (Mehlhorn et al.

1976).

Fig. 2.8 Life cycle of S. hominis and S. suihominis

2.9 Sarcocystosis 31

Control: Avoid consumption of raw or under-cooked pork or beef.

2.10 Toxoplasmosis

Subclass: CoccidiaOrder: EucoccidioridaFamily: Sarcocystidae

2.10.1 Synonyms

Congenital toxoplasmosis.

2.10.2 Etiology

Toxoplasmosis is a coccidial disease whichoccurs due to the parasite Toxoplasma gondii.

2.10.3 Reservoir

T. gondii is a protozoan parasite offlies with manyintermediate hosts, e.g. sheep, goat, pig, cattle,etc., including man (Dubey and Beattie 1988).

2.10.4 Epidemiology

Toxoplasmosis in man and sheep is prevalentworldwide including India (Dubey and Beattie1988; Dubey 1987; Chhabra and Mahajan 1982).In the first national serological prevalence ofT. gondii in India (Dhumne et al. 2007), 23,094serum samples were tested for T. gondii IgG andIgM antibodies using a solid-phase immunocap-ture ELISA. Antibodies IgG and IgM were foundin 24.3 and 2 % samples, respectively. The lowestseroprevalences were reported from the northern

Fig. 2.9 Transmission electron microscopy of S. cruzi,thin walled S. cruzi showing zoites in the granulomataand hair-like projections on the cyst wall (with kindpermission from Dr. Alvin A Gajadhar, Research Scien-tist cum Head, Centre for Food-Borne and AnimalParasitology, Canadian Food Inspection Agency Saska-toon Lab, Canada)

Fig. 2.10 Ultrastructure of Sarcocyst wall showingvillar projections (VP) arising from the S. cruzi cystwall. No microtubules are seen in VP and a zone ofground substance (GS) can also be seen (with kindpermission from Dr. Alvin A Gajadhar, Research Scien-tist cum Head, Centre for Food-Borne and AnimalParasitology, Canadian Food Inspection Agency Saska-toon Lab, Canada)

Fig. 2.11 Thick-walled Sarcocystis cyst in diaphrag-matic muscles of pig (H & E stain, 40X)

32 2 Protozoonoses

parts of the country, with the highest in the south.The data probably indicate the effects of signifi-cantly drier conditions and their related negativeimpact on the survivability of T. gondii oocysts innorthern India. It has also been observed that theseroprevalence of T. gondii in humans in India islow compared to that of western countries (Dubeyand Beattie 1988). Many other workers have alsoreviewed human toxoplasmosis in India (Parija2004; Dubey 1987).

2.10.5 Transmission

Human beings can become infected either aftereating raw or undercooked contaminated meatinfected with cysts of the parasite or from catfaeces infected with T. gondii oocysts. Theinfection can further be transmitted from aninfected mother to the foetus through the pla-centa. Although rare, organ transplant frominfected persons could also lead to infection.Transplacental transmission may also take place.Persons with weakened immune systems are athigh risk of being infected. Cat acts as thedefinitive host and shed oocysts in the faeces.The sporulated oocysts can be ingested by man,animals and mice (Fig. 2.12).

2.10.6 Clinical Signs in Man

In healthy persons, the disease is generallyasymptomatic. The symptoms generally appear7–14 days after the exposure. The parasite caninfect many vital organs such as brain, eye, liver,lung and heart. Symptoms generally includeheadache, fever, enlarged lymph nodes, partic-ularly of the neck and sore throat, and musclepain. In congenital toxoplasmosis, eye infectioncould lead to blindness. Congenital toxoplas-mosis could lead to mental retardation, multipleorgan failure, hydrocephalus or foetal death(Hohlfeld et al. 1989). Toxoplasmic encephalitis(TE) is the most frequent cause for focal nervoussystem disorder complicating AIDS. There havebeen various reports of TE from India (Chaddha

et al. 1999). Although Toxoplasma infectiondoes not cause repeated foetal losses, this is themost common indication for investigation oftoxoplasmosis in India.

2.10.7 Clinical Signs in Animals

The parasite remains asymptomatic most of thetime. The disease is particularly important insheep and goat where it may lead to abortions inpregnant animals. Congenital infections can alsooccur with young ones having problems inmuscle coordination.

2.10.8 Diagnosis

In intermediate hosts, the disease can be diag-nosed by molecular and serological tests, miceinoculation, histological and other tests such asMRI, CT scan, etc. Giemsa-stained microscopicexamination of impression smears can also bedone. In cat (definitive host), faecal examinationusing flotation techniques or serological testscan be performed (Figs. 2.13, 2.14).

2.10.9 Control

For prevention of the disease, consume properlycooked meat. Persons involved in slaughteringshould handle raw meat carefully and wash theirhands properly. Children should avoid access tocat faeces, particularly in playgrounds and parks.Pregnant women should not handle cat litter.

2.11 Other Protozoan ZoonoticDiseases

2.11.1 Cyclosporiasis

Cyclosporiasis occurs due to coccidium parasiteCyclospora cayetanensis. The human disease isworldwide in occurrence. The occurrence of thedisease in animals is unknown. The parasite

2.10 Toxoplasmosis 33

Fig. 2.12 Life cycle of Toxoplasma gondii

Fig. 2.13 Toxoplasma cyst, toludine stained (100 X)(with kind permission from Dr. Alvin A Gajadhar,Research Scientist cum Head, Centre for Food-Borne andAnimal Parasitology, Canadian Food Inspection AgencySaskatoon Lab, Canada)

Fig. 2.14 Transmission electron microscopy showingultrastructure of Toxoplasma cyst (with kind permissionfrom Dr. Alvin A Gajadhar, Research Scientist cum Head,Centre for Food-Borne and Animal Parasitology, Cana-dian Food Inspection Agency Saskatoon Lab, Canada)

34 2 Protozoonoses

could cause watery diarrhoea in human subjects.The double-walled oocysts can be detected infaeces using oocyst concentration and stainingtechniques (Fig. 2.15).

2.11.2 Infections Caused by Free-LivingAmoebae

The free-living amoebae belonging to the genusNaegleria, Acanthamoeba and Balamuthia couldcause the disease in man and some other mam-mals. The parasite Naegleria fowleri could causeamoebic meningoencephalitis in man. Acantha-moeba spp. could cause granulomatous amoebicencephalitis in man. The important sources ofinfection include contaminated water and soil.

2.11.3 Malaria in Non-human Primates

The disease occurs due to parasites belonging tothe genus Plasmodium (Phylum Apicomplexa)which affect non-human primates. Mosquitoesbelonging to the genus Anopheles act as vectorsof the disease. The infection due to plasmodia ofnon-human primates has been rarely recorded inhuman beings.

2.11.4 Microsporidiosis

The disease primarily occurs due to Enterocyto-zoon bieneusi, Encephalitozoon intestinalis,E. cuniculi and some other species. Microsporid-iosis is an important disease in immunodeficientindividuals. The important symptoms in maninclude diarrhoea and watery stools. Contamina-tion of water with infected faeces and stools couldserve as a source of infection for other persons.

2.11.5 Atypical HumanTrypanosomiasis

Although the zoonotic potential of trypanosomi-asis in humans due to animal trypanosomes is notcertain, 19 (T. lewisi-8, T. evansi-5, T. brucei-4,T. vivax-1, T. congolense-1) atypical human try-panosomiasis cases have been reported in theliterature (Joshi 2013).

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Simo G, Asonganyi T, Nkinin SW, Njiokou F, Herder S(2006) High prevalence of Trypanosoma bruceigambiense group 1 in pigs from the Fontem sleepingsickness focus in Cameroon. Vet Parasitol139:57–66

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Singh BB (2001) Prevalence and immunodiagnosis ofSarcocystis sp. of public health signifance in cattle.M.V.Sc. Thesis, Punjab Agricultural University,Ludhiana

Singh BB, Sharma JK, Juyal PD, Aulakh RS (2003)Prevalence and comparative morphology of Sarco-cystis species recovered from cattle in Punjab. J ResPAU 40(3–4):456–458

Singh BB, Sharma JK, Juyal PD, Gill JPS (2004)Seroprevalence of Sarcocystis species of cattle inPunjab. J Vet Parasitol 18(1):75–76

Singh BB, Sharma R, Kumar H, Banga HS, Aulakh RS,Gill JPS, Sharma JK (2006) Prevalence of Cryptos-poridium parvum infection in Punjab (India) and itsassociation with diarrhea in neonatal dairy calves. VetParasitol 140(1–2):162–165

Singh BB, Sharma R, Sharma JK, Banga HS, Kumar H,Aulakh RS, Gill JPS (2008) Prevalence of Giardiaintestinalis infection in cattle. J Vet Parasitol22(2):91–92

Singh R (2002) Prevalence and immunodiagnosis ofSarcocystis sp. of public health significance in swine.M.VSc Thesis, Punjab Agricultural University,Ludhiana

Stalheim OH, Fayer R, Hubbert WT (1980) Update onbovine toxoplasmosis and sarcocystosis with empha-sis on their role in bovine abortions. J Am Vet MedAss 176:299–302

Stephens JWW, Fantham HB (1910) On the peculiarmorphology of a trypanosome from a case of sleepingsickness and the possibility of its being a new species(T. rhodesiense). Proc R Soc Lond B 83:28–33

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Sutherst RW (1993) Arthropods as disease vectors in achanging environment. In: Lake JV, Bock GR,Ackrill K (eds) Environmental change and humanhealth. Ciba Foundation Symposium. AcademicPress, London, pp 124–145

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40 2 Protozoonoses

3Trematode Zoonoses

Abstract

Trematode zoonoses could be defined as ‘‘those trematode diseases whichare naturally transmitted between (other) vertebrate animals and man’’.Many neglected trematode zoonotic diseases are being considered asimportant human infections. The penetration of human skin by cercariae ofavian schistosomes leads to cercarial dermatitis. Metagonimus yokogawaiand Heterophes heterophes are the important heterophyids which couldcause zoonotic disease. Pigs appear to be natural definitive host forGastrodiscus hominis, which causes disease in human beings. Fasciolosisis mainly important in livestock but human cases have been reported from42 countries. The parasite Fasciolopsis buski is prevalent in manySoutheast Asian countries. Accidental ingestion of ants infected withDicrocoelium dendriticum could cause human disease. Among all the liverflukes, Clonorchis sinensis is the most important fish-borne zoonosesprevalent in East Asia. The parasite Paragonimus westermani is found inAsia, Africa and South America. In Africa, the public health burden ofschistosomiasis, caused by Schistosoma mansoni, S. hematobium andS. intercalatum is enormous.

3.1 Cercarial Dermatitis

Subclass: DigeneaFamily: Schistosomatidae

3.1.1 Common Name/Synonyms

Schistosome dermatitis, Swimmer’s itch, ricefarmer’s itch or clam digger’s itch

Cercarial dermatitis occurs due to penetra-tion of human skin generally with cercariae ofavian schistosome parasites. The diseaseoccurs across the globe mostly near freshwaterhabitats. Swimmer’s itch is a commonnon-communicable water-borne disease andhas been recently regarded as an emerginginfection (De Gentile et al. 1996; Kolarova2007). Cercarial dermatitis is an occupationalzoonosis in certain populations.

B. B. S. Dhaliwal and P. D. Juyal, Parasitic Zoonoses,DOI: 10.1007/978-81-322-1551-6_3, � Springer India 2013

41

3.1.2 Etiology

The disease primarily occurs due to larvae of 20species of Schistosome genera such as Aus-trobilharzia, Dendritobilharzia, Gigantobilharzia,Trichobilharzia and Orientobilharzia.

3.1.3 Epidemiology

Cercarial dermatitis is trematode zoonosis andworldwide in occurrence (Farahnak and Essalat2003). The disease has been reported from manycountries in Europe and America (De Gentile et al.1996; Bastert et al. 1998; Folster-Holst et al. 2001;Kolarova et al. 1999; Chamot et al. 1998; Lind-blade 1998). The parasite has also been detected insnails in Germany (Loy and Haas 2001). The caseshave been reported in North America, Canada,Europe, Africa, the Far East (Hoeffler 1977;Mulvihill and Burnett 1990) and Taiwan (Wangand Chang 2008). Several outbreaks of cercarialdermatitis have also been reported in Quebec,Canada, Germany, France, Thailand and along theHuaihe River of China (Levesque et al. 2002;Kullallavanijaya and Wongwaisayawan 1993;Verbrugge et al. 2004; Li et al. 1998).

The schistosome larvae develop in freshwatersnails leading to association of the disease in lakesor ponds where cercariae of bird schistosomes areusually reported as the causative agent of thedisease (Horák et al. 2002; Kolarova 2007). Fewoutbreaks from salt or brackish waters have alsobeen reported (Horák et al. 2002; Kolarova 2007).

3.1.4 Reservoir

The cercaria’s normal hosts are birds, rodents andvarious other small mammals and human beingsact as an accidental host (Wang and Chang 2008).

3.1.5 Transmission

Humans become infected when cercariae presentin water bodies attach and enter through the skinof the human accidental host.

3.1.6 Life Cycle

The adult parasites live in the mesenteric bloodvessels of birds or mammals and produce eggswhich are released in faeces of the host. Theeggs released through faeces into the waterbodies hatch and release miracidia. The mira-cidia penetrate an appropriate species of inter-mediate snail host. In snail they further developinto multiple sporocysts. Numerous fork-tailedcercariae develop in the snail host throughasexual multiplication (Bastert et al. 1998;Folster-Holst et al. 2001; Farahnak and Essalat2003). The cercariae are released in the waterwhere they penetrate a vertebrate definitive oraccidental (Brant et al. 2010) host’s skin usingoral suckers and release a proteolytic enzymewhich facilitates their penetration (Wang andChang 2008).

3.1.7 Clinical Signs in Man

The clinical disease was first reported by Fujiiin 1887 (Oda 1973). The schistosome larvae(cercariae) were identified as the causativeagent by Cort in 1928 in the USA. Thisfollowed the reporting of the causative agentsfrom United Kingdom (Matheson 1930) andFrance (Brumpt 1931). Christensen and Green(1928) used the word swimmers’ itch for thedisease. Clinical signs in man include a strongmaculo-papulovesicular skin eruption andintensive itching affecting areas exposed towater (Horák et al. 2002; Kolarova 2007).

The cercaria of non-human schistosomiasiscould occasionally penetrate the epidermis, butare unable to reach the bloodstream and toinduce systemic infection (Haas and van deRoemer 1998; Wang and Chang 2008). Theseparasites induce Type I hypersensitivity reactionand finally die due to histolysis (Wang andChang 2008). The residual cercarial proteincould induce Type IV hypersensitivity reactionand diffused skin eruptions (Kourilova et al.2004).

42 3 Trematode Zoonoses

3.1.8 Clinical Signs in Animals

Although cercarial dermatitis is mainly related tohuman infections, symptoms have been reportedin animals such as rabbits and dogs (Herber1938; Augustine and Weller 1949; Olivier 1953).

3.1.9 Diagnosis

History of exposure to the contaminated fresh-water and clinical signs give preliminary indi-cation for the disease (Scrimgeour and Daar2000). The parasite could be detected bymicroscopic observation of schistosome larvaefrom water snails (Kolarova 2007).

3.1.10 Control

Use of personnel protective measures could helpprevent the disease in human beings.

3.2 Dicrocoeliasis

Subclass: DigeneaOrder: PlagiorchiidaFamily: Dicrocoeliidae

3.2.1 Common Name/Synonyms

Lancet liver fluke disease

3.2.2 Etiology

The disease occurs due to D. dendriticum andD. hospes. The parasite resides in the bile ducts ofsheep, cattle and other mammals including man.

3.2.3 Epidemiology

The parasite is distributed in Europe (Mediterra-nean area), Asia (Middle East, Indonesia, Japan,Malaysia, People’s Republic of China), former

Soviet Union, North Africa, South America andsome foci in North America (Jeandron et al. 2011;Le Bailly and Bouchet 2010). Although theinfection is common in livestock, it has been rarelyreported in human beings (Jeandron et al. 2011).Human infections by D. dendriticum, a zoonoticliver fluke are not common and rare in occurrence.Most reports concern autochthonous populationsin Europe, Middle East and immigrants fromNorth Africa (Gualdieri et al. 2011; Ashrafi 2010).D. dendriticum has also been reported in humansfrom Canada (Schweiger and Kuhn 2008).Samalia et al. (2009) reported the disease in a7-year-old child presented with recurrent rightflank subcutaneous nodules containing a liverfluke on excision, and tissue histology showedcharacteristic brown operculated ova of D. den-driticum. El-Shafie et al. (2011) reported zoonoticdicrocoeliasis among a farmer’s family and hisdomestic animals. The human infection is mainlyasymptomatic or subclinical, but clinical cases ofhuman dicrocoeliasis have also been reportedfrom different parts of the world, including Iran(Ashrafi 2010) and Turkey (Cengiz et al. 2010).Cases of dicrocoeliasis in patients infected withthe human immunodeficiency virus (HIV) havealso been reported (Drabick et al. 1988; Zaliet al. 2004). D. dendriticum eggs have also beenfound in the stool of a patient with Crohn’s disease(Schweiger and Kuhn 2008). In Egypt, Helmyand Al-Mathal (2003) found that 121/1196patients were positive for D. dendriticum.

3.2.4 Reservoir

D. dendriticum is a small lancet fluke infectingdomestic and wild ruminants (e.g., buffalo, cattle,goat, sheep and deer), rabbits, and, occasionally,dogs, horses, pigs and humans. The parasite isfound in the small bile duct and gall bladder of themammalian host (Jeandron et al. 2011).

3.2.5 Transmission

Humans become infected after accidental inges-tion of infected ants (containing the metacercariae)

3.1 Cercarial Dermatitis 43

present on fruits, vegetables, grass or in drinkingwater (Haridy et al. 2003).

3.2.6 Life Cycle

Life cycle of the parasite involves two interme-diate hosts’ viz. land snails and ants (Fig. 3.1).

3.2.7 Clinical Signs in Manand Animals

The disease is generally asymptomatic in humanbeings. The clinical signs and pathology isgenerally similar to other liver trematodes suchas Clonorchis sinensis, Fasciola hepatica, and

Opisthorchis viverrini, and may include chronicdiarrhoea, constipation, right upper abdominalpain, vomiting, weight loss and fatigue(Jeandron et al. 2011). Hepatomegaly, peripheraleosinophilia, biliary obstruction and cholangitiscould also occur (Rana et al. 2007; Jeandronet al. 2011). Acute urticaria (Singh et al. 2008)has also been reported.

3.2.8 Diagnosis

The disease is difficult to diagnose from clinicalsigns. The disease can be diagnosed by identi-fication of the parasite eggs in the faecal sam-ples, while a living or dead fluke could be rarelyseen.

Fig. 3.1 Life cycle of Dicrocoelium dendriticum

44 3 Trematode Zoonoses

3.2.9 Control

Control of intermediate host population viz.snail and ants, health education can help in theprevention of the disease.

3.3 Echinostomiasis

Subclass: DigeneaFamily: Echinostomatidae

3.3.1 Common Name/Synonyms

Echinostomatidiasis

3.3.2 Etiology

These are intestinal parasites which can infectbirds and mammals. There are 15 species whichcan infect humans (Chai et al. 2005a, b;Yamashita 1964; Huffman and Fried 1990).Echinostoma hortense, Echinochasmus japoni-cus, E. echinatum are important species from 11fish-borne echinostomes (Chai et al. 2005a, b;Yu and Mott 1994; Chai and Lee 2002; Carney1991; Ujiie 1963).

3.3.3 Epidemiology

Human infections have been reported from Asia,Western Pacific and Africa (Chai et al. 2005a, b;Yu and Mott 1994; Haseeb and Eveland 2002).E. hortense has been reported from humans androdents in the Republic of Korea (Chai and Lee2002) and China (Yu and Mott 1994; Yu et al.1994). The parasite is endemic in Southeast Asiaand the Far East, i.e. mainland China, Taiwan,India, Korea, Malaysia, Philippines and Indonesia(Fried et al. 2004; Bandyopathy and Nandy 1986).

3.3.4 Life Cycle

Freshwater snail act as first intermediate hostwhere cercariae develop and may encyst asmetacercariae in another snail, mollusk, tadpoleor freshwater fish (second intermediate hosts)(Acha and Szyfres 2006).

3.3.5 Transmission

Ingestion of raw or undercooked second inter-mediate host (fish) can cause infection in humanbeings.

3.3.6 Clinical Signs in Man

The symptoms are generally related to the levelof parasitemia (Fried et al. 2004; Bandyopathyand Nandy 1986; Chai et al. 1994). Clinical signsare generally not evident but ulcerations andbleeding in the stomach or duodenum may occurin E. hortense infection (Chai et al. 1994). Inlight to moderate infections, anaemia, headache,dizziness, slight stomach ache, gastric pain andloose stools have been reported (Chattopadyayet al. 1990; Bundy et al. 1991). Heavy infectionsare associated with eosinophilia, abdominal pain,profuse watery diarrhoea, anaemia, oedema andanorexia (Chattopadyay et al. 1990). Severeulcerative lesions with bleeding in the duodenumhave also been reported in some cases (Chai et al.1994).

3.3.7 Clinical Signs in Animals

The experimental infections in rats have lead todecrease in villus/crypt ratio, villous atrophy,crypt hyperplasia and inflammation of thestroma (Chai et al. 2005a, b; Chai and Lee2002).

3.2 Dicrocoeliasis 45

3.3.8 Diagnosis

The disease can be diagnosed by identificationof characteristic operculate, non-embryonated,ellipsoidal, yellow to yellow–brown eggs and bythe morphology of the adult parasite (Fried et al.2004; Bandyopathy and Nandy 1986). Inrodents, the infections can be diagnosed on thebasis of serological tests (Graczyk and Fried1994, 1995; Graczyk 1997).

3.3.9 Treatment

Praziquantel @ 10–20 mg/kg in a single oralregimen can be used to treat the infections (Chaiand Lee 2002).

3.3.10 Control and Prevention

The human disease can be controlled by inter-rupting the life cycle of the parasite (Graczykand Fried 1998). Avoiding consumption of rawor undercooked meat of molluscs, fish, crusta-ceans and amphibians can help prevent the dis-ease in humans (Graczyk and Fried 1998).

3.4 Fascioliasis

Subclass: DigeneaSuperfamily: Fasciolidae

3.4.1 Common Name/Synonyms

Sheep liver fluke disease

3.4.2 Etiology

The disease occurs due to liver fluke F. hepaticaand F. gigantica.

3.4.3 Epidemiology

The fascioliasis is mainly important in livestock(Malek 1980; Boray 1982). Human cases havebeen reported from 42 countries (Chen and Mott1990; Esteban et al. 1998; Mas-Coma et al.1999a, b) and up to 2.4 million people arebelieved to be infected with this parasite (Rim1994; WHO 1995a). F. hepatica mainly occursin Europe, Asia, Africa, Americas and Oceania.F. gigantica has been reported in Asia and Africa(Ashrafi et al. 2006). Human fascioliasis isbecoming an important public health problemthese days (Chen and Mott 1990; WHO 1995b;Mas-Coma et al. 1999a, b). Health problems dueto human fascioliasis have been reported in manycountries such as Bolivia, Peru, Chile, Ecuador,Cuba, Egypt, Portugal, France and Spain and Iran(Mas-Coma et al. 2004, 2005a, b).

3.4.4 Transmission

Sheep and cattle mainly act as reservoir hosts forF. hepatica. The infection in human beings canoccur directly through drinking contaminatedwater or through ingestion of contaminatedfreshwater plants or vegetables (Chen and Mott1990; Mas-Coma et al. 1999a; Cadel 1996).

3.4.5 Life Cycle

The parasite needs two hosts to complete theirlife cycle. The definitive hosts mainly includeherbivorous animals such as sheep, cattle andhuman beings. In the definitive hosts, eggs passthrough bile duct and are excreted in the faeces.Eggs develop outside the host to miracidialstage. Miracidia enters the freshwater snails. Thesnails of the family Lymnaeidae act as inter-mediate hosts. Miracidia develop to rediae in thesporocyst which further develop to cercariaewhich swim in water and attaches to freshwateraquatic plants. Encystation of cercaria occursand humans and other definitive hosts become

46 3 Trematode Zoonoses

infected after ingestion of infective metacerca-riae (Mas-Coma et al. 2005a, b) (Fig. 3.2).

3.4.6 Clinical Signs in Animals

There is development of haemorrhagic tracts,swelling in the liver. Fibrosis of the liver couldresult in bile duct blockage and inflammationwhich can result in death during chronic phaseof the disease. The occurrence of submandibularoedema (Bottle jaw) is a typical symptomnoticed in fasciolosis.

3.4.7 Clinical Signs in Man

Hepatic involvement results in inflammation andswelling of the liver. Additional symptomsinclude abdominal pain, anaemia, fever, chole-cystitis and cholelithiasis.

3.4.8 Diagnosis

The disease can be diagnosed through clinicalsigns, identification of the eggs, during PMexamination and by immunological tests.

3.4.9 Control

Prevention and control of animal fasciolosis,vector population can help control the disease inhuman beings (Roberts and Suhardono 1996;Torgerson and Claxton 1999; Spithill et al.1999). Avoid ingestion of contaminated plants inendemic areas.

3.5 Fasciolopsiasis

Subclass: DigeneaFamily: Fasciolidae

Fig. 3.2 Life cycle of Fasciola hepatica

3.4 Fascioliasis 47

3.5.1 Etiology

The disease occurs due to F. buski, which is thelargest fluke affecting human being (Kuntz andLo 1967).

3.5.2 Epidemiology

The parasite is prevalent in many countries ofsouth and East Asia including Thailand, China,Taiwan, Vietnam, Bangladesh and India(Mas-Coma et al. 2005a, b; Lo and Lee 1996;Wiwanitkit et al. 2002; Gilman et al. 1982; Leet al. 2004). Fasciolopsiasis has been reviewedin detail by Mas-Coma et al. (2005a, b).

3.5.3 Reservoir

Pigs act as important reservoirs of infection(Rim 1982a, b, c).

3.5.4 Transmission

Human beings become infected through ingestionof metacercariae by drinking contaminated wateror due to consumption of infected plants. Fascio-lopsiasis generally occurs near freshwater habitatswith stagnant or slow moving waters (Mas-Comaet al. 2005a, b). Cultivation of freshwater plantsand pollution with human and animal (mainly pig)excreta are important factors for the transmissionof the disease (Mas-Coma et al. 2005a, b).

3.5.5 Life Cycle

The adult parasite is present in the intestine of thehuman and pig host. The parasite inhabits duo-denum and jejunum but could be found in otherparts of the intestinal tract in heavy infections.Eggs released in the faeces embryonate in waterin 3–7 weeks (Weng et al. 1989). After hatching,miracidia infect snails of the genera Segmentina,Hippeutis and Gyraulus which shed cercariaeafter 4–6 weeks (Graczyk et al. 2000). Cercariae

encyst on the surface of freshwater plants (Wenget al. 1989). Ingestion of metacercariae lead toinfection in human and pig hosts.

3.5.6 Disease in Man

High morbidity occurs due to fasciolopsiasis inendemic areas (Graczyk et al. 2001; Weng et al.1989) and the disease may become fatal in heavyinfections (Graczyk et al. 2001 and Weng et al.1989). In light infections, anaemia, headache,dizziness, stomach ache, gastric pain and loosestools (Gilman et al. 1982) may be seen. Heavyinfections could result in severe epigastric andabdominal pain, diarrhoea or bowel obstruction,nausea, acute ileus, anasarca and markedeosinophilia and leucocytosis (Gilman et al.1982). Malnutrition (Graczyk et al. 2001; Wenget al. 1989) is an important factor associatedwith heavy infections.

3.5.7 Diagnosis

The disease may be diagnosed by faecal sampleexamination for presence of eggs and adultparasite (Mas-Coma et al. 2005a, b). Moleculartechniques could also be used in future.

3.5.8 Control

Control can be achieved by proper diagnosis,treatment of people and livestock, preventingreinfection and instituting modern pig farmingand avoiding consumption of freshwater plants(Mas-Coma et al. 2005a, b).

3.6 Gastrodisciasis

Subclass: DigeneaFamily: Paramphistomatidae

3.6.1 Common Name/Synonyms

Gastrodiscoidosis, Amphistomiasis

48 3 Trematode Zoonoses

3.6.2 Etiology

Gastrodiscoides species are approximately8–14 mm in length (Fried et al. 2004).Gastrodiscoides hominis causes disease in humanbeings. The parasite has a pharynx, tandem, lobedtestes, a post-testicular ovary, an ascendinguterus and a ventral genital pore (Kumar 1999).

3.6.3 Epidemiology

The parasite has been reported primarily fromIndia but cases have been reported fromBangladesh and East Asian countries (Acha andSzyfres 2006).

3.6.4 Transmission

The transmission of the disease occurs when rawor undercooked vegetation, crustaceans, mol-luscs or amphibians contaminated with encystedmetacercariae are consumed.

3.6.5 Clinical Signs in Manand Animals

Swine appears to be natural definitive host. Thedisease condition associated with G. hominis isalso referred to as gastrodisciasis. The flukesexcyst from metacercariae and descend in theintestinal tract to reach the cecum and colonwhere they mature and live as adults (Kumar1999). The parasite infects humans and hogs,e.g. hogs in Africa (Goldsmid 1975; Hira 1983)and India (Murty and Reddy 1980). Disease isgenerally inapparent but could cause mucoiddiarrhoea (Strickland 1991).

3.6.6 Diagnosis

Morphological identification of trematode flukeand detection of parasite eggs in faecal samplescan help in diagnosis of the disease.

3.7 Heterophyiasis

Subclass: DigeneaFamily: Heterophyidae

3.7.1 Common Name/Synonyms

Heterophyes infection

3.7.2 Etiology

Heterophyids are minute intestinal flukesbelonging to the family Heterophyidae (Chaiet al. 2005a, b). These parasites infect birds andmammals (Chai et al. 2005a, b). Although 35heterophyid species can infect man (Chai et al.2005a, b), but from zoonotic point of view,Metagonimus yokogawai and Heterophyesheterophyes are the important species (Yu andMott 1994). Studies have been carried out fromPhilippines (Belizario et al. 2001) and Thailandon Haplorchis taichui (Waikagul 1991;Sukontason et al. 2001) and from Korea on sev-eral species including Heterophyes nocens andMetagonimus species (Chai and Lee 1991; Chaiand Lee 1990, 2002; Chai et al. 2005a, b). Aquaticsnails and fresh or brackish-water fish acts as firstand second intermediate hosts, respectively.

3.7.3 Metagonimiasis

The genus Metagonimus is identified by a lat-erally deviated ventral sucker and absenceof ventrogenital apparatus or genital sucker(Chai and Lee 2002).

3.7.3.1 EtiologyThe disease occurs due to M. yokogawai,Metagonimus takahashii, M. minutus andMetagonimus miyatai.

3.7.3.2 TransmissionThe molluscan freshwater snail acts as an inter-mediate host (Chai and Lee 2002). The species

3.6 Gastrodisciasis 49

has rather broad fish host specificity, but thesweet fish Plecoglossus altivelis is an importantfish host in Korea and Japan (Chai et al. 2005a, b).

3.7.3.3 EpidemiologyThe disease is endemic in Korea (Chai et al.1977; Seo et al. 1981; Chai and Lee 2002; Chaiet al. 1993). The human infections have alsobeen recorded from Siberia, Europe, China,Japan, Russia and Taiwan (Chai et al. 2005a, b;Yu and Mott 1994; Ito et al. 1991).

3.7.3.4 Clinical Signs in ManThe parasite affects the mucosa of the middle partof the small intestine (Chai 1979) and could leadto villous atrophy, crypt hyperplasia and inflam-matory reactions (Chai 1979). Gastrointestinalproblems such as epigastric pain, diarrhoea,anorexia and fatigue could occur in mild infec-tions. Heavy infections may lead to abdominalcramps, malabsorption and weight loss.

3.7.3.5 DiagnosisThe disease may be diagnosed by identificationof the parasite eggs by faecal examination.

3.7.3.6 TreatmentPraziquantel @ dose of 10–20 mg/kg orally maybe used for treatment of the infection (Chai andLee 2002).

Other Metagonimus species

Other Metagonimus species infecting humansinclude M. takahashii Suzuki (Chai and Lee2002) and M. miyatai (Saito et al. 1997; Chaiand Lee 2002) which can be differentiated fromM. yokogawai using PCR-based-restrictionfragment length polymorphism (PCR–RFLP)patterns, karyotypes, simple sequence repeat-PCR (SSR–PCR) patterns (Chai and Lee 2002)and amplification of mitochondrial cytochrome coxidase subunit I and 28S ribosomal DNAsequences (Lee et al. 2004).

3.7.4 Heterophyiasis Dueto Heterophyes Species

The genus Heterophyes is characterised by themedian location of the ventral sucker and thepresence of a genital sucker armed with gonotyl(Chai and Lee 2002).

3.7.4.1 EtiologyThe disease occurs due to Heterophyiasis het-erophyes (v. Siebold, 1852, Stiles and Hassall,1900), Heterophyes dispar and H. nocens (syn.Heterophyes katsuradai), (Yu and Mott 1994;Chai et al. 1986; Chai and Lee 2002). The adultflukes measure 1.0–1.7 mm long, 0.3–0.4 mmwide, and possess large median ventral suckerand a genital sucker with gonotyl armed with60–90 multidigitate spines (Beaver et al. 1984).

3.7.4.2 EpidemiologyThe adult parasites are found in fish-eating birdsand mammals in addition to humans (Radomyoset al. 1994; Kumar 1999). The parasite is frag-mented in distribution in parts of the world (Chaiet al. 2005a, b; Yu and Mott 1994). Humandisease has been recorded from Egypt, Japan(Kagei et al. 1980) and Republic of Korea (Chaiet al. 1986; Chai and Lee 2002).

3.7.4.3 TransmissionConsumption of raw, undercooked or inade-quately processed freshwater, brackish or marinefishes (Radomyos et al. 1994) and mullet Mugilcephalus (Yu and Mott 1994) are importantsources of infection.

3.7.4.4 Life CycleDogs, cats, foxes, jackals and other fish-eatingmammals act as important reservoirs (Radomyoset al. 1994). Pirenella conica and Cerilbida cengu-lata are the important gastropod first intermediatehosts of these heterophyids. The second intermedi-ate hosts include brackish-water fishes in the genusMugil (mullets), Aphanius and Acanthogobius.

50 3 Trematode Zoonoses

3.7.4.5 Clinical Signs in Animalsand Man

The disease is generally asymptomatic but highparasitemia could lead to irritation of intestinalmucosa, increased mucus, chronic diarrhoea,colic and nausea (Acha and Szyfres 2006).Aberrant eggs may produce granulomatous foci inmyocardium and brain (Acha and Szyfres 2006).

3.7.4.6 DiagnosisMorphological identification of adult fluke anddetection of parasite eggs in faecal samples canhelp in diagnosis (Radomyos et al. 1994).

3.7.4.7 Prevention and controlControl measures include avoidance of eatingraw or undercooked fish, personnel hygienemeasures, treatment of infected people, envi-ronmental sanitation, proper excreta disposaland disease awareness.

3.7.5 Haplorchiasis

Haplorchis species have a single testis and ventro-genital sucker complex with gonotyl and chitinousspines (Chai et al. 2005a, b; Yamaguti 1958).Human disease can occur due to H. taichui,Haplorchis pumilio, Haplorchis yokogawai,Haplorchiasis pleurolophocerca and Haplorchisvanissimus (Yu and Mott 1994; Chai et al. 2005a, b);the first three parasites are the most important (Chaiet al. 2005a, b). The Haplorchis species are foundthroughout Asia (Velasquez 1982) among humans.H. taichui Chen 1936 was first reported from birdsand mammals from central Taiwan (Faust andNishigori 1926). H. pumilio is distributed in Asia(Velasquez 1982; Yu and Mott 1994) in birds andmammals. H. yokogawai human infections havealso been reported from many Asian countries,Australia and Egypt (Velasquez 1982; Yu and Mott1994).

3.8 Nanophyetus

Subclass: DigeneaFamily: Troglotrematidae

3.8.1 Common Name/Synonyms

Salmon poisoning (in animals), Elokomin flukefever

3.8.2 Etiology

The disease occurs due to trematode flukeNanophyetus salmincola Chapin, 1927 (syn.Troglotrema salmincola Witenberg 1932)belonging to the family Nanophyetidae (Chaiet al. 2005a, b). Nanophyetus schikhobalowi, isanother species described from natives of far-eastern Siberia and is regarded as a subspeciesN. salmincola schikhobalowi (Millemann andKnapp 1970; Kumar 1999).

3.8.3 Epidemiology

Eastburn et al. (1987) recorded 10 cases ofNanophyetus from North West America. Ferrelet al. (1974) also detected cases of Nanophyetussalmincola in kippered salmon in America. Thedisease is endemic in the far-eastern part ofRussia (Yu and Mott 1994). In USA, the prev-alence in local ethnic minorities could reach upto 60 % (Eastburn et al. 1987).

3.8.4 Life Cycle

The snail Oxytrema silicula acts as the firstintermediate host in USA and Semisulcospiracancellata and S. laevigata in Siberia. The sal-monid (trout, salmon) and non-salmonid fish(Millemann and Knapp 1970) act as secondintermediate hosts. The non-embryonated eggsare released in the faeces of the mammalianhost. Miracidia develop within the egg in about4 months and hatches and penetrates in the firstintermediate host. Cercariae develop and emergefrom the snail to penetrate skin and gills ofsalmonid fish. This is followed by encystation inthe muscles and connective tissues of secondintermediate host (Fried et al. 2004). The adultparasite develops in the intestine of definitive

3.7 Heterophyiasis 51

host after consumption of infected fish (Schell1985). The adult resides in the small intestine ofmammals (Schell 1985).

3.8.5 Reservoir

The fishes Oncorhynchus species, Salmo spe-cies, Cottus perplexus, Dicamptodin ensatus andSalvelinus fortinalis transmit the infection tohumans in the United States (Fried et al. 2004).

3.8.6 Transmission

Consumption of raw or undercooked infectedfish is an important source of infection.

3.8.7 Clinical Signs in Man

Clinical signs include gastrointestinal symptomssuch as peripheral blood eosinophilia, increasedfrequency of bowel movements or diarrhoea,abdominal discomfort, nausea, vomition, weightloss and fatigue (Eastburn et al. 1987).

3.8.8 Clinical Signs in Animals

The parasite can infect different mammalsincluding dogs, cat, raccoon and foxes. The par-asite also affects three species of birds on thePacific coast of North America, Canada andEastern Siberia (Chai et al. 2005a, b; Millemannand Knapp 1970; Beaver et al. 1984). In dogs,foxes and coyotes, this fluke is particularlyimportant as it acts as the vector of a rickettsia,Neorickettsia helmintheca, which causes a seriousand often fatal systemic infection known as ‘sal-mon poisoning’, which has not been reported inhumans (Chai et al. 2005a, b). The mortality due torickettsia in dogs may reach 90 % (Schell 1985).

3.8.9 Diagnosis

The disease can be diagnosed by detection ofeggs typical for N. salmincola from stool

samples. Eggs of the parasite are operculate andnot embryonated.

3.8.10 Control

Avoid eating raw or undercooked fish.

3.9 Other Liver Flukes

Subclass: DigeneaFamily: Opisthorchiidae

These liver flukes belong to the familyOpisthorchiidae. These include clonorchiasis,opisthorchiasis and Metorchis infections. Theseparasites generally have similar life cycles andsymptoms (Chai et al. 2005a, b). As per WHO,17 million people are infected with liver flukes(WHO 1995a, b, c).

3.9.1 Clonorchiasis

3.9.1.1 Common Name/SynonymsChinese Liver fluke disease

3.9.1.2 EtiologyThe disease occurs due to C. sinensis. Among allthe liver flukes, C. sinensis is the most importantfish-borne zoonosis prevalent in East Asia (Chaiet al. 2005a, b; Rim 1990; Chen et al. 1994;Hong 2003; Yoshida 2012).

3.9.1.3 EpidemiologyThis parasite causes serious disease in manyparts of the world (Chai et al. 2005a, b) partic-ularly in China, Japan, Korea and countries ofSoutheast Asia (Shekhar et al. 1995).

3.9.1.4 ReservoirThe cats, dogs and pigs are believed to act asreservoirs but their role as reservoirs has notbeen well studied (Chen et al. 1994; WHO1995a, b, c).

52 3 Trematode Zoonoses

3.9.1.5 TransmissionThe definitive hosts become infected throughconsumption of raw or undercooked infectedfish.

3.9.1.6 Life CycleThe parasite lives in the biliary tract of defin-itive host (man and fish-eating animals) andsheds eggs through bile duct and intestines(Chai et al. 2005a, b). Freshwater snails(Parafossarulus manchouricus and otherhydrobid snails) ingest these eggs. The mira-cidia hatches in the snail and develop intosporocysts (Rim 1982a). Rediae are formedwithin the sporocyst and cercariae furtherdevelop within the rediae (Chai et al. 2005a, b;Kaewkes 2003). In water, free swimming cer-caria penetrates beneath the fish’s scales and istransformed into an encysted metacercaria(Chai et al. 2005a, b). Many species of thefreshwater fishes and shrimp can act as thesecond intermediate host (Chen et al. 1994;Park et al. 2004). The metacercariae developinto the adult in the definitive host (Rim 1986).Humans and fish-eating mammals and birds canact as definitive hosts (Fig. 3.3).

3.9.1.7 Clinical Signs in Animalsand Man

Most important symptoms include calculi for-mation, cholangitis, cholecystitis and cholan-giohepatitis. Infection of pancreas could lead topancreatitis or obstruction of pancreatic duct.Chronic infections can also lead to cholangio-carcinoma (Flavell 1981; Chai et al. 2005a, b).

3.9.1.8 DiagnosisThe disease can be diagnosed by multiple stoolexaminations for identification of parasite eggsin faeces. The eggs may also be diagnosed fromduodenal aspirates. Specialised techniques suchas cellophane thick smear (Chai et al. 1982) orKato-Katz techniques (Hong et al. 2003) may beused. Serological tests such as ELISA may alsobe done (Choi et al. 2003).

3.9.1.9 ControlThe prevention and control relies on avoidingconsumption of raw or undercooked fish, vectorcontrol and prompt diagnosis and treatment ofthe infection.

3.9.2 Opisthorchiasis

Four species of the parasite viz. O. viverrini,Opisthorchis felineus, O. noverca and O. guaya-quilensis could infect humans (Kaewkes 2003).Out of these, O. viverrini is prevalent in SoutheastAsia (Chai et al. 2005a, b; Shekhar et al. 1995)and particularly causes serious disease (Chai et al.2005a, b; Rim 1982b; Kaewkes 2003). O. felineusis a parasite of dogs, cats, foxes and pigs in Europeand the Asiatic parts of Russia, Turkey andSiberia (Chai et al. 2005a, b; Beaver et al. 1984;Rim 1982b). The life cycles, symptoms anddiagnosis are similar to that of C. sinensis.

3.9.3 Metorchiosis (Canadian LiverFluke)

The disease occurs due to Metorchis conjunctus.The parasite is found in carnivorous animals

in Canada and USA (MacLean et al. 1996).Human infections have also been reported inCanada (Yamaguti 1958; MacLean et al. 1996;Behr et al. 1998). Mode of transmission, symp-toms are similar as for other liver fluke infec-tions (Rim 1982b; Beaver et al. 1984).Carcinoma of the infected parts may lead todeath in some cases.

3.10 Paragonimiasis

Subclass: DigeneaFamily: Troglotrematidae

3.10.1 Common Name/Synonyms

Lung fluke disease, pulmonary distomatosis,endemic hemoptysis and oriental hemoptysis.

3.9 Other Liver Flukes 53

3.10.2 Etiology

The disease primarily occurs due to Paragoni-mus westermani, lung fluke belonging to thefamily Troglotrematidae. Paragonimus skrjabiniis another species found in China but few para-sites develop into adult in man (Liu et al. 2008).

3.10.3 Epidemiology

The parasite is found in Asia, Africa and SouthAmerica. The disease has been recorded frommany countries such as China, Japan, Liberia,Nigeria and Venezuela (Obara 2004; Liu et al.2008).

3.10.4 Reservoir

The disease could occur in carnivorous animalssuch as tiger, lion, dogs, cats, pigs and non-human primates.

3.10.5 Transmission

Human beings become infected after consump-tion of infected crabs or crayfish (Singh 1986).

3.10.6 Life Cycle

Humans and carnivores animals can act asdefinitive hosts for P. westermani. Intermediatehosts include snails (importantly species

Fig. 3.3 Life cycle of Clonorchis sinensis

54 3 Trematode Zoonoses

Semisulcospira, Melanopides) and crabs orcrayfish (Velez 2003). In humans and carnivoresanimals, lungs are important site of predilectionand harbour the adult parasite (Liu et al. 2008;Guan 2005). The eggs are coughed up from therespiratory system and passed in faeces. Con-tamination of freshwater with faeces of thedefinitive host leads to embryonation andhatching of the eggs. Free swimming miracidiaenters the first intermediate host. Miracidiadevelops to sporocyst to redia to cercaria in thefirst intermediate host. Crabs or cray fish ingeststhe snail and cercariae encysts and develops intometacercariae in the vessels of the gills, liverand muscles of the cephalothorax. Humans andcarnivores animals become infected after theingestion of raw or undercooked infected

crustacean host. Metacercariae excyst in intes-tinal tract and reach through abdominal cavity todiaphragm to pleural cavity and finally to thelungs (Obara 2004; Guan 2005) (Fig. 3.4).

3.10.7 Clinical Signs in Animals

The involvement of respiratory system may leadto formation of granulomata and abscess cavities.

3.10.8 Clinical Signs in Man

The respiratory system infections could result insymptoms such as chest pain, cough, blood-stained sputum and dyspnea. If gastrointestinal

Fig. 3.4 Life cycle of Paragonimus westermani

3.10 Paragonimiasis 55

system is infected, symptoms include abdominalpain, or diarrhoea and eggs can be seen in thestools (Waikagul 1989). Extrapulmonary para-gonimiasis mostly result in involvement ofcentral nervous system (Huang 2000).

3.10.9 Diagnosis

The disease may be diagnosed from clinicalsigns, detection of eggs from sputum or faecesand CT, MRI or serological techniques.

3.10.10 Control

Control measures include avoiding consump-tion of raw or undercooked crab or crayfish, control of intermediate host (snail) pop-ulations and avoiding contamination of surfacewater with faeces of definitive host (Liu et al.2008).

3.11 Schistosomiasis

Subclass: DigeneaOrder: StrigeididaFamily: Schistosomatidae

3.11.1 Common Name/Synonyms

Bilharziasis, snail fever

3.11.2 Etiology

The disease occurs due to Schistosoma haemat-obium (urinary schistosomiasis), S. mansoni,S. japonicum, S. mekongi and S. malayi, (gas-trointestinal and hepatosplenic schistosomiasis)and S. intercalatum, which also affects the GItract but with lower morbidity (Almeda et al.1994; Corachan 2002).

3.11.3 Epidemiology

More than 300 million people are believed to beinfected worldwide, the parasite being morecommon in children aged between 5 to 15 years(WHO 1993; Standley et al. 2009; Fenwick et al.2009). Schistosomiasis has been reported in mostAfrican countries, limited areas of SouthAmerica, Caribbean, Middle East and Asia(Corachan 2002; Standley et al. 2012; Hotez et al.2008). Schistosoma japonicum is the causativeagent of schistosomiasis in China, Philippinesand in small pockets of Indonesia (Gray et al.2008; Ross et al. 2001, 2002). In Africa,the public health burden of schistosomiasis,caused by S. mansoni, S. haematobium andS. intercalatum/guineensis, is enormous (Hotezand Fenwick 2009). The losses occurring due tohuman schistosomiasis caused by S. mansoni,S. haematobium and S. japonicum have beenestimated to be 1.7–4.5 million disability adjustedlife years (McManus et al. 2010) (DALYs). Thetrue burden was found to be substantially greaterthan previous estimates (Finkelstein et al. 2008;Jia et al. 2007; King et al. 2005; Van der Werfet al. 2003). In China, zoonotic schistosomiasisjaponica, also called ‘‘snail fever,’’ is a significanthealth risk for human and livestock populations(McManus et al. 2010, 2009; Ross et al. 2001;Utzinger et al. 2005; Wang et al. 2006; Zhou et al.2005, 2007).

3.11.4 Reservoir

The zoonotic nature of S. japonicum furthercomplicates parasite transmission and control. Theparasite has ability to infect more than 40 speciesof wild and domestic animals (WHO 1993). Ear-lier studies indicated public health importance ofrats, dogs, pigs, sheep and goats, cattle and waterbuffalo hosts (Johansen et al. 2000; WHO 1993).In China, however, water buffaloes (Bubalusbubalis) could play a significant role in the trans-mission of S. japonicum (Johansen et al. 2000;WHO 1993; Gray et al. 2008).

56 3 Trematode Zoonoses

3.11.5 Transmission

Human beings become infected after exposure tofreshwater containing cercariae released by theinfected snails (Corachan 2002). Snails act asthe intermediate host for the parasite (Corachan2002).

3.11.6 Life Cycle

Freshwater infected with free-swimmingcercariae is important source of infection. Thecercariae penetrate the skin of humans and manyother animals, including water buffaloes, sheep,pigs, cattle, rodents and dogs, which can act as

Fig. 3.5 Life cycle of Schistosoma species

3.11 Schistosomiasis 57

important reservoirs for human infection (Rosset al. 2001; Zhou et al. 2007) (Fig. 3.5).

3.11.7 Clinical Signs in Man

The disease is generally asymptomatic in humanbeings. In infections due to S. japonicum,S. mansoni; early lesions occur in small intestinefollowed by portal hypertension due to Schisto-soma eggs retained in the portal spaces, ascitisand spleenomegaly. Clinical symptoms due toS. haematobium schistosomiasis include hae-maturia, proteinuria and leukocyturia accompa-nied by dysuria and nocturia (Corachan 2002).Chronic infections could lead to obstructiveuropathy and hydronephrosis (Corachan 2002).S. japonicum infection may lead to fever,headache and lethargy, portal hypertension,ascites and hepatosplenomegaly, which cancause premature death (Ross et al. 2002).

Rare CNS involvement due to embolization ofeggs to the brain and spinal cord may occur inS. japonicum and S. mansoni infections (Alfred1996). Early infection in childhood can causegrowth retardation and anaemia (Ross et al. 2002).

3.11.8 Clinical Signs in Animals

The disease is common in animals. The symp-toms generally are similar to as that in man.

3.11.9 Diagnosis

The disease can be diagnosed by detection of eggsin human stool samples, tissue biopsy examina-tions or ultrasonography (Corachan 2002), clini-cal signs, serologicalormolecular techniques. Theeggs of S. japonicum are round and have a shellwith reduced lateral spine (McManus et al. 2010).

3.11.10 Control

Control measures include health education,control of snails, water hygiene and treatment ofinfected cases.

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4Cestode Zoonoses

Abstract

Cestode Zoonoses could be defined as ‘‘those cestode diseases which arenaturally transmitted between (other) vertebrate animals and man.’’ Thezoonotic cestodes belonging to family Taeniidae are of paramountimportance in the developing world. Most of the food producing animalsviz. cattle, buffalo, sheep, goat and pigs along with some other mammalsact as intermediate hosts for Echinococcus granulosus. Human beingscould become infected after accidental consumption of Echinococcusspecies eggs shed in the faeces of the definitive carnivorous host/animal.Taeniasis is a true zoonotic infection (Euzoonoses) where pig and cattleact as intermediate host for Taenia solium and Taenia saginata,respectively and human beings act as definitive/final hosts. Neurocystic-ercosis is an important public health issue and is responsible forneurological disorders worldwide. Besides important animal and humanhealth concern; the economic losses arising due to these infections areenormous. Coenurosis is a rare zoonosis and more than 100 human caseshave been reported across the globe. Other important cestodes includeparasites such as Diphyllobothrium latum and Spirometra mansoni.Different epidemiological trends have been reported across the globe fordiphyllobothriasis. The parasite Dipylidium caninum can cause disease indomestic dogs, cats, some wild carnivores and occasionally man.Sparganosis is a rare cestode zoonosis that can infect man. The parasitehas been recorded across the globe but is commonly found in easternAsia. The important cestodes transmitted through food and waterincludes T. solium, E. granulosus and D. latum.

B. B. S. Dhaliwal and P. D. Juyal, Parasitic Zoonoses,DOI: 10.1007/978-81-322-1551-6_4, � Springer India 2013

65

4.1 Coenurosis

Order: CyclophyllideaFamily: Taeniidae

4.1.1 Common Name/Synonyms

Gid, Sturdy, Vertigo

4.1.2 Etiology

The intermediate stages (larval forms) of theparasites Taenia multiceps, Taenia serialis andT. brauni viz. Coenurus cerebralis, C. serialis,C. brauni, respectively are responsible for thedisease in intermediate hosts including man.

4.1.3 Epidemiology

Coenurosis is a rare zoonosis and more than 100human cases have been reported across the globe(Scala and Varcasia 2006). Human coenurosis israre in occurrence but cases have been reported

from Africa, Asia, Europe and America(Johnstone and Jones 1950; Templeton 1971;Ing et al. 1998; Scala and Varcasia 2006; Beniflaet al. 2007; El-on et al. 2008).

4.1.4 Life Cycle

The human disease occurs due to the larval formof T. multiceps. The canids (dogs, foxes, coyotes)act as the definitive host for T. multiceps and theherbivorous animals primarily sheep, act asintermediate hosts. For T. serialis, lagomorphsand rodents act as intermediate hosts. Wildrodents act as intermediate hosts for T. brauni.Humans could act as accidental intermediatehosts after ingestion of eggs of the parasite presentin the faeces of the definitive host (Fig. 4.1).

4.1.5 Clinical Signs in Man

In human beings, the cysts (larval forms) havebeen found in CNS, eye and other tissues andsymptoms vary depending upon the location andsize of the cyst.

Fig. 4.1 Life cycle of Taenia multiceps

66 4 Cestode Zoonoses

4.1.6 Clinical Signs in Animals

In sheep, the parasite affects nervous system andcysts are found in CNS resulting in nervoussymptoms which may lead to death of the animalafter few weeks. The disease can also occur ingoat, cattle and horses.

4.1.7 Diagnosis

The disease can be diagnosed in humans usingcomputed tomography and magnetic resonanceimaging. In definitive host, disease can bediagnosed by identification of the parasite(Figs. 4.2 and 4.3).

4.1.8 Control

Control of stray dogs, avoiding free access ofthese stray animals to slaughter waste, dewor-ming of the definitive host and improved

personnel hygiene can help prevent the diseasein human beings.

4.2 Diphyllobothriasis

Subclass: CestodaOrder: Pseudophyllidea

4.2.1 Common Name/Synonyms

Fish tapeworm infection, Bothriocephaliasis

4.2.2 Etiology

The disease occurs due to the tapeworm of thespecies Diphyllobothrium. Diphyllobothriumlatum is the most important species responsiblefor human zoonosis followed by D. dendriticum,Diphyllobothrium dalliae, DiphyllobothriumKlebanovskii, Diphyllobothrium nihonkaienseand few other species (Scholz et al. 2009).

4.2.3 Epidemiology

The parasite is found in cold water areas ofEurope, Asia, North and South America and hasalso been reported from Japan, Russia, Koreaand many other countries (Dick et al. 2001).There is a decline in prevalence of the diseasefrom North America, Asia and Europe (Scholzet al. 2009) and reemergence from countriessuch as Russia, South Korea, Japan and SouthAmerica has been reported (Scholz et al. 2009).Among humans,D. latum and D. dendriticum have been reportedfrom holarctic region, and from circumpolarareas and South America, respectively (Torreset al. 2004). Other species such as D. nihonka-iense, D. klebanovskii, and Diphyllobothriumpacificum have been recorded in Japan, easternEurasia and along the Pacific Coast of SouthAmerica (Chai et al. 2005). These parasites havealso been reported from Middle East andMalaysia (Abo-Shehada and Ziyadeh 1991;

Fig. 4.2 Coenrus cyst in thigh muscle of goat

Fig. 4.3 Borax carmine stained multiple scolices ofT. multiceps

4.1 Coenurosis 67

Rohela et al. 2002), Republic of Korea (Leeet al. 2001). Domestic animals, especially dogs(Adams and Rausch 1997; Torres et al. 2004)and faecal contamination of waterbodies (Lloyd1998; Cross 2001; Torres et al. 2004; Dupouy-Camet and Peduzzi 2004) also help to completelife cycle of the parasite (Dick et al. 2001).Although decline in human disease has beenobserved, but the parasite is prevalent in theother hosts and is a permanent risk for humaninfection (Dick et al. 2001; Chai et al. 2005).

4.2.4 Transmission

In man, the disease occurs due to consumptionof raw or undercooked fish containing the ple-rocercoid stage of the parasite.

4.2.5 Life Cycle

The eggs are released into the faeces of thedefinitive host (man and other fish eatingmammals). The eggs hatch in the water to formcoracidium (Von Bonsdorff 1977). The cora-cidium is ingested by copepod which acts as thefirst intermediate host (Eguchi 1973; Magath1937; Torres et al. 2007). Procercoid develops inthe first intermediate host (Chervy 2002). Fish(second intermediate host) become infected afterthe ingestion of infected copepod (first inter-mediate host). The plerocercoids develop fromprocercoid in the tissues of the fish (Chervy2002). Ingestion of raw or improperly cookedfish containing plerocercoids (larval stages) leadto the infection in carnivore mammals/fish-eat-ing birds/human beings (Bylund and Andersen1994). The parasite requires three hosts forcompletion (Rausch and Adams 2000) of its lifecycle. Parasite could develop at different tissuesin the fish depending upon the species of theparasite involved (Dick et al. 2001) (Fig. 4.4).

4.2.6 Clinical Signs in Man

Most of the times, disease remains asymptom-atic or cause mild symptoms such as abdominaldiscomfort and diarrhoea. Clinically, the parasitemay cause megaloblastic anaemia due to defi-ciency of vitamin B12.

4.2.7 Clinical Signs in Animals

The disease normally remains asymptomatic indogs and cats but very severe infection couldlead to death.

4.2.8 Diagnosis

The disease can be diagnosed by identificationof the eggs of the parasite (ovoid shape, oper-culum on narrow pole, 35–80 by 25–65 lm), orusing PCR.

4.2.9 Control

The disease can be controlled by breaking thelife cycle of the parasite. Avoid contaminationof water bodies. Prompt treatment of infectedcases and consumption of properly cooked fishcould help prevent the infection in humanbeings. Sewage to be discharged in water bodiesmust be properly treated before discharge.

4.3 Dipylidiosis

Order: CyclophyllideaFamily: Dilepididae

4.3.1 Common Name/Synonyms

Dog tapeworm infection

68 4 Cestode Zoonoses

4.3.2 Etiology

The disease occurs due to Dipylidium caninum(cyclophyllidean cestode). The parasite D.caninum (Linnaeus 1758, Cyclophyllidea,Dipylidiidae) can cause disease in domesticdogs, cats, some wild carnivores, and occasion-ally human beings (Schmidt and Roberts 2000).

4.3.3 Epidemiology

The disease occurs across the globe and humancases have been reported in many Europeancountries, India, China, Japan, etc. The humaninfection mostly occurs in young children asthey often play with dogs and cats (Marx 1991).

Fig. 4.4 Life cycle of Diphyllobothrium latum

4.3 Dipylidiosis 69

4.3.4 Life Cycle and Transmissionin Man

Intermediate hosts include cat and dog(Ctenocephalides felis and Ctenocephalidescanis) flea but dog lice (Trichodectes canis andHeterodoxus spiniger) and human flea (Pulexirritans) can also transmit the parasite (Craigand Ito 2007; Chappell and Penn 1990).Definitive hosts (dogs and cats) become infec-ted after ingestion of the flea and lice infectedwith cysticercoids (Robertson and Thompson2002). Accidental infection occurs in humanbeings after ingestion of the infected cat anddog flea or food contaminated with infectedflea (Turner 1962). The intermediate hostsbecome infected after ingesting contaminatedanimal faeces (Fig. 4.5).

4.3.5 Clinical Signs in Man

The disease has been reported from infants andyoung children (Tsumura et al. 2007; Reddy1982; Claudia et al. 2003; Reid et al. 1992). Inhuman beings, the disease is rarely seen and

often remains asymptomatic but symptoms suchas abdominal pain, diarrhoea and increasedirritability of anus and intestinal obstruction maybe seen. Proglottids (rice grain like) are excretedin the faeces of the host.

4.3.6 Clinical Signs in Animals

The infection generally remains asymptomaticin dogs, but few typical signs such as crawlingand rubbing around the anus could result due toperianal pruritus (Dantas-Torres 2008). Pro-glottids (rice grain like) can also be seen aroundperianal area (Dantas-Torres 2008).

4.3.7 Diagnosis

The disease can be diagnosed after microscopicidentification of parasite eggs or observing ricegrain-like proglottids in faeces. The gravid pro-glottids contain eggs packed in embryonicmembrane. The eggs are 20–40 lm in diameterand contain a hexacanth embryo (Neira et al.2008; Ramana et al. 2011).

Fig. 4.5 Life cycle of Dipylidium caninum

70 4 Cestode Zoonoses

4.3.8 Control

Control of the flea vectors from dog, cat and theirsurroundings, personnel hygiene (washing handsof children after they play with pets), proper dis-posal of cat and dog faeces and regular dewor-ming of pet animals can help control the infection.

4.4 Echinococcosis

Class: CestodaOrder: CyclophyllideaFamily: Taeniidae

4.4.1 Common Name/Synonyms

Hydatidosis, dwarf dog tapeworm

4.4.2 Etiology

Echinococcosis is a very important cestodezoonosis. The infection occurs due to the para-sites belonging to the species Echinococcus(Family Taeniidae). E. granulosus, Echinococ-cus multilocularis, Echinococcus oligarthrusand Echinococcus vogeli (Rausch 1975 andThompson 1995) are the species of the genusEchinococcus responsible for the disease.Among these, E. granulosus zoonosis is partic-ularly significant due to many domestic, man-made life-cycle patterns and involvement ofnumber of intermediate hosts (Eckert 1998;Schantz et al. 1995). Further, there are ninerecognised strains of E. granulosus (Thompsonet al. 1995). The metacestode infection is com-monly known as hydatidosis.

4.4.3 Epidemiology

E. granulosus is worldwide in occurrence(Eckert et al. 2001; Singh et al. 2012a, b, Juyalet al. 2005; Bhatia and Pathak 1990) and human

cases have been reported throughout the worldwhereas E. multilocularis is mainly prevalent innorthern hemisphere. The other two parasites arefound in central and south America (Acha andSzyfres 2006).

4.4.4 Transmission

The carnivorous animals act as definitive hosts,and shed eggs in their faeces. The ingestion ofthese eggs by the intermediate host animals andoccasionally man leads to development of met-acestode stage in their visceral organs primarilyliver and lungs (WHO and OIE 2001).

4.4.5 Life Cycle

Most of the food producing animals viz. cattle,buffalo, sheep, goat and pigs along with someother mammals act as intermediate hosts forE. granulosus (Rausch 1986; Rausch 1995;Thompson and Allsopp 1988; WHO 1984).Dog and foxes act as definitive hosts forE. granulosus and E. multilocularis, respectivelyfor most of the times.

E. granulosus—Definitive host: Dogs and wildcanidsIntermediate host: Sheep, pig, cattle, buffalo,goat, horses, camels, other herbivorous animalsand manE. multilocularis—Definitive host: Arctic fox(Alopex lagopus) and red fox (Vulpes vulpes)Intermediate host: Wild rodentsE. oligarthrus—Definitive host: Wild felids(Jaguars, Pumas etc.)Intermediate host: RodentsE. vogeli—Definitive host: Wild canid (Speothosvenaticus)Intermediate host: Rodent Cuniculus paca

Life cycle of other Echinococcus species isalmost similar to E. granulosus involving theirrespective intermediate and definitive hosts(Fig. 4.6).

4.3 Dipylidiosis 71

4.4.6 Clinical Signs in Man

Human beings could become infected afteraccidental consumption of eggs of the parasiteshed in the faeces of the definitive carnivoroushost/animal. Depending upon the parasiteinvolved, three types of the disease could occurin human beings (WHO and OIE 2001).

Cystic echinococcosis (CE): The diseaseoccurs due to metacestode of E. granulosus.C. echinococcosis is an important disease prob-lem in many parts of the world (WHO and OIE2001). Unilocular cysts occur in liver, lung andfew other organs.

Alveolar echinococcosis (AE): The diseaseoccurs due to metacestode of E. multilocularisand produces alveolar hydatidosis. Althoughrare, but disease is malignant and highly fatalamong infected human beings.

Polycystic echinococcosis (PE): The diseaseoccurs due to metacestode of E. vogeli orE. oligarthrus.

The clinical signs in these forms varydepending upon the type of visceral organinvolved. Liver and lungs are parasitised most ofthe times and the related clinical signs are seenaccordingly.

4.4.7 Clinical Signs in Animals

4.4.7.1 Intermediate HostsThe symptoms generally do not appear and thedomestic animals remain asymptomaticthroughout their life, but the disease causessignificant economic losses in most of the foodproducing animals at the time of slaughter due to

Fig. 4.6 Life cycle of Echinococcus granulosus

72 4 Cestode Zoonoses

condemnation of infected organs. Large-sizedhydatid cysts can cause symptoms in the animalsdue to pressure atrophy of the affected organ(s)(Schwabe 1986). The cysts are mainly found inliver and lung but can be present in spleen, heart,kidney and other organs (Orlando 1997; WHOand OIE 2001). The cysts are responsible forreduced growth and milk production especiallyin dairy animals.

4.4.7.2 Definitive HostThe infected carnivorous animals generally donot present any clinical symptoms.

4.4.8 Diagnosis

In intermediate host animals, the disease can bediagnosed at the time of post mortem inspectionof the infected organs, radiographic techniques,ultra sonography, PCR and serological tech-niques. In carnivorous animals, detection of eggsusing conventional parasitological techniquesand later confirmation by PCR and serologicaltechniques can be used. In human beings, radi-ography along with serological confirmation isroutinely used for diagnosis of the parasite(Figs. 4.7, 4.8, 4.9, 4.10, 4.11, 4.12 and 4.13).

4.4.9 Control

Control of stray dogs, prevention of illegalslaughter (with free access to dogs) and treatmentof infected dogs are important steps to be takenFig. 4.7 Hydatid cysts in liver of sheep

Fig. 4.8 Hydatid cysts in lungs of sheep

Fig. 4.9 Hydatid cysts in liver of pig

Fig. 4.10 Fully mature invaginative forms of protosco-lices at 10 X

4.4 Echinococcosis 73

particularly for the control of E. granulosusrelated echinococcosis.

4.5 Sparganosis

Subclass: CestodaOrder: PseudophyllideaFamily: Diphyllobothriidae

4.5.1 Common Name/Synonyms

Spirometrosis, Larval diphyllobothriasis

4.5.2 Etiology

Several species of the Spirometra, such asSpirometra mansoni, S. mansonoides andS. erinaceieuropaei can cause the disease.

4.5.3 Epidemiology

Sparganosis is a rare cestode zoonosis that caninfect man. The parasite has been recordedacross the globe but is commonly found ineastern Asia (Viroj 2005) viz. countries such asChina, Korea, Japan, and from Southeast Asia.The parasite has also been reported from adomestic cat in India (Saleque et al. 1989).

4.5.4 Life Cycle

Humans can act as accidental secondary inter-mediate host where plerocercoid (metacestodestage) develop and results in sparganosis(Beaver et al. 1984; Andersen 1983; Cho et al.1990; Tesacharoen 1980). Frogs act as thesecond intermediate hosts. Ingestion of larvaefrom cyclops (copepod; first intermediate host)or frogs can lead to infection in humans, pigsand mice (Fukushima and Yamane 1999;Nithiuthai et al. 2004). Second stage larvae(spargana) during their migration in these hosts(reptiles-snakes; mammals such as pigs andhuman beings) cause the disease (Mueller 1974;Bearup 1953; Daly 1982; Acha and Szyfres1987). The animals belonging to the familycanidae and felidae act as definitive hosts(Fig. 4.14).

4.5.5 Transmission

The disease is transmitted to man throughingestion of infected copepods in drinking water,

Fig. 4.11 Alternate arrangement of large and smallhooks in the rostella (E. granulosus) at 100X

Fig. 4.12 Taenia spp. eggs seen at 10X

Fig. 4.13 Taenia spp. eggs at 100X

74 4 Cestode Zoonoses

ingesting lightly cooked frogs and snakes,poultry and pork. Use of infected frog as abandage and pressing it on the ulcers, skin andeye could lead to transmission of the parasitethrough mucous membranes (Mueller 1974;Acha and Szyfres 1987).

4.5.6 Clinical Signs in Man

The spargana can enter brain, eye, subcutaneoustissues, abdominal cavity, and rarely spinal cordwhich can result in blindness, paralysis anddeath (Yoon et al. 2004; Cho et al. 2000). Theparasite has the ability to infect cerebral, ocular,subcutaneous and other visceral organs depend-ing upon the migration of the parasite (Holodniyet al. 1991).

4.5.7 Clinical Signs in Animals

The infection generally remains asymptomaticin intermediate and definitive hosts but couldcause weight loss and emaciation in cats.

4.5.8 Diagnosis

The disease can be diagnosed from clinicalsigns, identification of parasitic stages andserological tests.

4.5.9 Prevention and Control

For preventing the disease, clean drinking waterand properly cooked meat of the concernedspecies should always be consumed.

Fig. 4.14 Life cycle of Spirometra species

4.5 Sparganosis 75

4.6 Taeniasis and Cysticercosis

Order: CyclophyllideaFamily: Taeniidae

Taeniasis is a true zoonotic infection(Euzoonoses) where pig and cattle act as inter-mediate host for Taenia solium and Taeniasaginata, respectively and human beings act asdefinitive hosts. Taenia asiatica (from pigs),much related to T. saginata could also infecthuman beings (Li et al. 2007).

4.6.1 Common Name/Synonyms

T. solium taeniasis, T. saginata taeniasis, cysti-cercosis, measly pork, measly beef, neurocys-ticercosis (NCC)

4.6.2 Etiology

The infection occurs due to T. solium andT. saginata in pigs and cattle, respectively. Thelarval forms of T. solium and T. saginata areknown as Cysticercus cellulosae and C. bovis inpigs and cattle, respectively.

4.6.3 Epidemiology

T. saginata, T. solium, and T. asiatica are pre-valent worldwide. Taeniasis swine is an impor-tant public health issue particularly indeveloping countries (Pathak et al. 1984; Juyalet al. 2008) and 20 million persons are believedto be infected with T. solium cysticerci (Bernet al. 1999) and as per WHO, adult parasites areprevalent among 2 million people worldwide(Shandera et al. 1994; White 2000; Yanagidaet al. 2012; Del Brutto 1999; Murrell 2005).Neurocysticercosis is an important public healthissue and is responsible for neurological disor-ders worldwide (White 2000; Flisser et al.2005). T. asiatica is distributed in east Asia(Anantaphruti et al. 2007).

4.6.4 Transmission

Humans and pigs act as definitive and interme-diate hosts, respectively for T. solium. But acci-dental ingestion of eggs of the parasite(T. solium) by human beings can also lead toserious disease such as neurocysticercosis.So both the taeniasis and cysticercosis due toT. solium can occur in human beings. Humanbeings become infected after ingestion of raw orpartially cooked measly pork (Singh et al. 2002).Pigs and human beings can become infected afteringestion of eggs shed by human carriers. Tae-niasis infected person (Taenia carriers) act asimportant risk factor for neurocysticercosis forthe other members of the family (Flisser 1994).Poor sanitary conditions and feeding of pigs ongarbage and human waste are important factorsresponsible for the spread of the disease (Li et al.2007; Sarti et al. 1992; Pawlowski and Murrell2001; Burneo and Garcia 2002). Sewage farmingis another important risk factor for neurocystic-ercosis even for the vegetarians and non-porkeaters. The consumption of measly beef couldlead to T. saginata taeniasis in man (Fig. 4.15).

4.6.5 Clinical Signs in Man

The important symptoms due to taeniasis includeabdominal pain, nausea, diarrhoea but the diseasemay remain asymptomatic at times (Garcia et al.2003). But the prompt diagnosis of T. solium tae-niasis is important so as to avoid the risk of auto-infection through faecal contamination leading toneurocysticercosis in human beings. In case ofcysticercosis, cysticerci may be present in the sub-cutaneous tissue beneath the skin, skeletal or cardiacmuscles. Rare eye infections leading to blindness(Cardenas et al. 1992) and tongue infections (Eliaset al. 2005) can also occur. The cysticerci havetendency to develop in the brain tissue leading toneurocysticercosis (Garcia et al. 2003). Dependingupon the location and number of cysticerci in thecentral nervous system, the symptoms such as sei-zures and headaches, vision problems, late-onset/

76 4 Cestode Zoonoses

adult/acquired epilepsy (Medina et al. 1990; White2000) and death can occur. T. saginata taeniasisusually remain asymptomatic but very high parasiteloads can result in abdominal pain, diarrhoea,weight loss and intestinal obstruction.

4.6.6 Clinical Signs in Animals

No symptoms are usually seen in pigs even ifthousands of cysts are present (Garcia et al.2003). Small cysts can be seen in many organssuch as skeletal muscles and some visceralorgans, but the disease generally remains

asymptomatic. However, T. solium cysticercosiscauses huge economic losses to the pig industry(Garcia et al. 2003).

4.6.7 Diagnosis

Detection of Taenia eggs from faecal samples,immunodiagnostic tools such as ELISA, coproantigen detection assays, CT and MRI can beused for diagnosis of the disease from humanbeings (Garcia et al. 2003; Allan et al. 2007).Cysticercosis is mainly diagnosed at the time ofpost mortem examination in pigs (Figs. 4.16,4.17, 4.18 and 4.19).

Fig. 4.15 Life Cycle of Taenia solium

4.6 Taeniasis and Cysticercosis 77

4.6.8 Control

Elimination of human carriers is highly impor-tant for prevention of neurocysticercosis (CDC1992). The T. solium carriers should be treatedwith anthelmintics such as praziquantel (Flisseret al. 2005; Garcia 2001). Interdisciplinaryapproaches (Engels et al. 2003), use of anthel-mintics (Roman et al. 2000) in endemic areas,avoiding free access of human faeces to pigs,education of lower socioeconomic populationcan help reduce the incidence of the disease(Juyal et al. 2008). Consumption of properlycooked pork, implementation of meat inspectionpractices and freezing of pork for appropriatetime before consumption can help prevent thedisease.

4.7 Other Cestode Zoonoses

4.7.1 Bertiellosis

Bertiellea species cestode commonly occurs inchimpanzees and rodents. The two speciesB. studri and B. macronata have also beenreported from human beings (Feldman et al.1983; Denegri and Perez-Serrano 1997; Denegriet al. 1998). Oribatid mites act as intermediatehost where cysticercoid stage occurs. Humanbeings can become infected after accidental

Fig. 4.17 Cysticercus cellulosae in striated muscles ofpig

Fig. 4.18 Cysticercus cellulosae in striated muscles ofpig

Fig. 4.19 Pig brain infected with Cysticercus cellulosae

Fig. 4.16 Cysticercus cellulosae in striated muscles ofpig

78 4 Cestode Zoonoses

ingestion of these mites. The disease remainsasymptomatic but there might be abdominalpain, diarrhoea and general fatigue in somehuman patients (Denegri and Perez-Serrano1997).

4.7.2 Hymenolepiosis

The disease occurs due to Hymenolepis nana orH. diminuta which have zoonotic significance(Waugh et al. 2006). Rodents act as principalhost for these parasites but the parasite couldinfect humans, particularly children (Goswamiet al. 2011). The parasite has been recorded frommany parts of the world (Marangi et al. 2003)particularly from India (Watwe and Dardi 2008).The life cycle of parasite is direct with theinfection through faecal oral route in humans, butrat may play role in the transmission of the dis-ease due to contamination of human food with ratfaeces. The parasite infects gastrointestinal sys-tem and remains asymptomatic but can causeabdominal pain, diarrhoea, weakness, etc.

4.7.3 Inermicapsiferosis

The infection occurs due to Inermicapsifermadagascariensis found in rodents in Africa(Acha and Szyfres 2006). The parasite rarelyinfects man through rodent-arthropod-man cycle(Acha and Szyfres 2006).

4.7.4 Mesocestoidosis

The disease occurs due to Mesocestoides linea-tus and M. variablis (Acha and Szyfres 2006).The parasite has been reported from Japan,China and Korea (Eom et al. 1992). The lifecycle of the parasite is not clear but dogs, catsand other carnivores may act as definitive hostand coprophagous arthropod as first intermediatehost and rodents, birds, amphibians, reptiles assecond intermediate host (Acha and Szyfres2006). Consumption of undercooked meat ofamphibians, reptiles, etc. may cause the disease

in man. The parasite infects gastrointestinalsystem and may cause abdominal pain, diar-rhoea, weakness, etc.

4.7.5 Raillietinosis

The infection occurs due to Raillietina celeb-ensis and Raillietina demerariensis and fewother species found in rodents. Insects act asintermediate hosts where cysticercoids developand rare human infections occur after acciden-tal ingestion of food contaminated with infectedarthropod (Acha and Szyfres 2006). The para-site generally remains asymptomatic but couldaffect circulatory, nervous or digestive systemin man.

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Singh BB, Sharma JK, Tuli A, Sharma R, Bal MS,Aulakh RS, Gill JPS (2012b) Prevalence and mor-phological chracterisation of Echinococcus granulo-sus from north India. J Parasitic Dis. doi:10.1007/s12639-012-0189-x

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82 4 Cestode Zoonoses

5Nematode Zoonoses

Abstract

Nematode Zoonoses could be defined as ‘‘those nematode diseases whichare naturally transmitted between (other) vertebrate animals and man’’.Zoonotic nematodes infect millions of people worldwide. An overview ofthe epidemiology, transmission, clinical manifestations and diagnosis ofzoonotic nematodes is presented, along with methods of prevention andcontrol. Angiostrongylosis is endemic in south Asia, Pacific islands,Australia, China and Caribbean islands. Zoonotic ascariasis due toAscaris suum has been widely reported in North America and someEuropean countries. Baylisascaris procyonis, the intestinal roundworm ofraccoons has been reported to cause severe neurologic disease in man.Subcutaneous migration of the animal hookworms could lead tocutaneous larva migrans (CLM) in man. Gnathostomiasis is a food-borne zoonosis of public health significance. Trichinellosis has beenreported in most parts of the world except the deserts. The provision ofsafe food and water in the non-industrialised countries is of utmostimportance for the prevention and control of these diseases.

5.1 Acanthocephalus

Phylum: AcanthocephalaFamily: Oligacanthorhynchidae

5.1.1 Common Name/Synonyms

MacracanthorhynchusThese parasites are spiny-headed worms and

at times are included in the same phylum

with nematodes (Garcia 2001). They are pseu-docoelomate endoparasites and have manyunique morphological and biological features(Marquards et al. 2000; Garcia 2001).

5.1.2 Etiology

Acanthocephalus primarily occurs due to fol-lowing species of parasites:

B. B. S. Dhaliwal and P. D. Juyal, Parasitic Zoonoses,DOI: 10.1007/978-81-322-1551-6_5, � Springer India 2013

83

5.1.3 Epidemiology

Acanthocephalus is not common and has beenrarely reported in man. Till date, seven cases ofacanthocephlus have been reported (Robertsand Janovy 2005; Berenji et al. 2007). Theseparasites include Acanthocephalus bufonis,Corynosoma strumosum, Acracanthorhynchuahirudinaceus, Moniliformis moniliformis, Bolb-soma sp. (Counselman et al. 1989; Marquardset al. 2000; Roberts and Janovy 2005), Macra-canthorhynchua ingens (Counselman et al. 1989,Roberts and Janovy 2005) and Acanthocephalusrauschi (Marquards et al. 2000; Roberts andJanovy 2005). The parasite M. moniliformis hasbeen reported from many parts of the world(Ikeh et al. 1992; Roberts and Janovy 2005).Human infections due to M. moniliformis havebeen reported from Africa, Asia, Australia,Europe, and America (Muller 1975; Beaver et al.1984; Ikeh et al. 1992; Baker et al. 2000; Berenjiet al. 2007). The morphological parameters ofthe parasite have been described in detail bydifferent authors (Lawlor et al. 1990; Beaveret al. 1984; Roberts and Janovy 2005).

5.1.4 Transmission

Man gets the infection after consumption of rawparatenic host (Roberts and Janovy 2005) or dueto incidental consumption of intermediate host(Berenji et al. 2007).

5.1.5 Life Cycle

Humans are the incidental hosts, and the wormresides in the small intestine. The definitivehosts become infected after eating the interme-diate host (Ikeh et al. 1992).

5.1.6 Clinical Signs in Manand Animals

The symptoms of the disease are not well defined.High parasitemia may lead to vomition, abdominalpain, perforation of the intestine, fatigue, diar-rhoea, anorexia, irritability and intermittent burn-ing sensations around the umbilicus (Beaver et al.1984; Counselman et al. 1989; Ikeh et al. 1992;

Name of the parasite Definitive host Intermediate host References

MacracanthorhynchushirudinaceusSynonym: Gigantorhynchushirudinaceus, G. gigas,Echinorhynchus gigas

Swine, wild boar and occasionallyrodents, bovine, dog, monkey and man

Dung beetle of thefamilyScarabaeidae

Acha andSzyfres(2006)

Moniliformis moniliformis Rats and small rodents Beetles andcockroaches

Corynosoma strumosum Arctic fox (Alopex lagopus), dog, seaotter (Enhydra lutris) and species ofcetaceans and pinnipeds

Amphipodcrustacean(Pontoporeiaaffinis)Many species offish could act asparatenic host

Acanthocephalus rauschi,A. bufonis (A. sinensis)

Crustaceans –

Bolbosoma spp. Cetaceans Juvenile state foundin fish

84 5 Nematode Zoonoses

Marquards et al. 2000; Roberts and Janovy 2005).The penetration of proboscis and release andreattach tendency of the parasite could lead toinflammation, ulcer and haemorrhages in thedefinitive host (Marquards et al. 2000; Garcia2001; Roberts and Janovy 2005). It has beenobserved that M. moniliformis infected cockroachmove more slowly and travel shorter distances(Moore et al. 1994; Libersat and Moore 2000;Roberts and Janovy 2005). This might be respon-sible for the parasite’s predation by the definitivehost (Libersat and Moore 2000). The morbidity isgenerally high among mammals infected withacanthocephalans. However, fish may remainasymptomatic even after high intensities of wormsdeeply penetrated into their intestinal wall(Taraschewski 2000). The high heavy metalsabsorbance capacity indicates the usefulness ofacanthocephalans as bioindicators (Taraschewski2000).

5.1.7 Diagnosis

The disease can be diagnosed by identificationof the thick-shelled eggs containing first larvalstage in the faecal samples, while a living ordead fluke is rarely seen.

5.1.8 Control

Humans should avoid ingestion of intermediateor paratenic host.

5.2 Angiostrongylosis

Order: StrongylidaSuperfamily: Metastrongyloidea

5.2.1 Common Name/Synonyms

Intestinal angiostrongyliasis, eosinophilic menin-gitis

5.2.2 Etiology

The rat lung worm, Angiostrongylus cantonensiswas first time reported in China (Chen 1935)from domestic rat. This is a food-borne zoonoticnematode parasite of significant public healthimportance. Angiostrongylus costaricensis cau-ses abdominal eosinophilic granulomas in Cen-tral and South America (Pien and Pien 1999).

5.2.3 Epidemiology

Angiostrongylosis due to A. cantonensis isendemic in south Asia, Pacific islands, Australia,China and Caribbean islands (Wang et al. 2008;Lv et al. 2008).

5.2.4 Transmission

Human beings become infected after consump-tion of intermediate (raw snails) or paratenichosts (freshwater prawns, crabs, frogs), or veg-etables contaminated with the infected larvae(Alicata 1991).

5.2.5 Life Cycle

For A. cantonensis, rats and molluscs act as thedefinitive and intermediate host for this parasite,respectively. The crustaceans (prawns and landcrabs), predacious land planarians (flatworms inthe genus Platydemus), frogs and monitor lizards(Wang et al. 2008) are the important paratenichosts. The parasite A. cantonensis is present in the(pulmonary arteries) rat lungs. Larvae hatch andmigrate through trachea and gastrointestinal tractto rat faeces. These first stage larvae are eaten upby snails and slugs, and further develop intoinfective larvae (third stage). Man and ratsbecome infected after consuming infected snail orcontaminated vegetables. Larvae migratetowards the brain in human beings and could leadto brain abscess and haemorrhage (Koo et al.1988). The parasite A. costaricensis resides inmesenteric arteries of caecum of cotton rat. The

5.1 Acanthocephalus 85

first stage larvae penetrate slugs and develop tosecond and third stage larvae. The cycle is com-pleted when definitive host ingest infective larvaereleased from slugs (Fig. 5.1).

5.2.6 Clinical Signs in Man

In A. cantonensis angiostrongylosis, the parasiteinfects brain (Cross 1978; Chotmongkol andSawanyawisuth 2002). The other importantsymptoms include headache, neck stiffness,paraesthesia, vomition and nausea (Wang et al.2008). Symptoms due to A. costaricensis includeabdominal pain, vomition and rarely gastroin-testinal bleeding (Hulbert et al. 1992; Silveraet al. 1989).

5.2.7 Clinical Signs in Animals

The infected rodents may show sneezing,coughing, fibrosis in the lungs and occasionallygastrointestinal lesions.

5.2.8 Diagnosis

The disease can be diagnosed after detection ofthe parasite from cerebrospinal fluid or ocularchamber (Wang et al. 2008). History, clinicalsigns and serological tests are also useful in thediagnosis. Diagnosis of human angiostrongylosis(A. cantonensis) is based on clinical features aswell as laboratory findings (Eamosobhana andYong 2009; Eamsobhana 2006).

5.2.9 Control

Prevention and control measures primarily relyupon health education, avoidance of eating rawor undercooked intermediate and paratenichosts, unwashed vegetables and rodent control.

5.3 Anisakiosis

Order: AscarididaFamily: Anisakidae

Fig. 5.1 Life cycle of Angiostrongylus cantonensis

86 5 Nematode Zoonoses

Anisakiosis is parasitic zoonosis whichoccurs due to accidental ingestion of the parasitelarvae (Sakanari and Mckerrow 1989).

5.3.1 Common Name/Synonyms

Herring worm disease, Cod worm disease

5.3.2 Etiology

The disease can occur due to Anisakis, Pseudo-terranova and Contracaecum species, butAnisakis is primarily important. A. simplex isparticularly associated with gastroallergic ani-sakiosis (Audicana et al. 2002).

5.3.3 Epidemiology

The scientist ‘Van Thiel’ for first time recognizedAnisakiosis in 1960 (Van Theil 1960). The dis-ease is common in Japan (about 2000 cases/year)but cases have also been recorded from northernEurope (Scandinavia, Holland) and Pacific coastof South America (Caramello et al. 2003). Gastricanisakiosis is more common in Japan, whileintestinal anisakiosis has been mainly reportedfrom Europe (Audicana et al. 2002).

5.3.4 Transmission

Human beings become infected after eating raw orlightly cooked marinated seafood such as Japanesesushi and sashimi, Dutch salted or smoked herring,Scandinavian gravlax, Hawaiian lomi–lomi andLatin American ceviche (Chai et al. 2005).

5.3.5 Life Cycle

The adult parasites are present in stomach ofmarine fish (whales and dolphins). Crustaceans

act as first intermediary hosts. Fish and somecuttlefish act as paratenic hosts (Caramello et al.2003). Human beings become infected afterconsumption of third stage larvae present ininfected salt-water fish or cephalopod molluscspecies, including mackerel, squid, sardine,horse mackerel, salmon and bonito (Yasunagaet al. 2010; Karasawa et al. 2008). In fish, larvaegenerally localise on the surface of visceralorgans, body cavity and occasionally on themuscles. In man, the parasites do not mature, butthey cause the disease. Other definitive hostsinclude birds, reptiles and amphibians (Fig. 5.2).

5.3.6 Clinical Signs in Man

The symptoms could arise due to both gastricand intestinal anisakiosis. Clinical signs arerelated to allergic reactions and tissue damage.Presence of Anisakis allergens in the humanfood cause gastroallergic anisakiosis which maylead to urticaria, angioedema and anaphylacticshock associated with other gastrointestinalsymptoms (Caramello et al. 2003; LopezSerrano et al. 2000). Acute gastric anisakiosisoccurs suddenly 12–72 h after ingestion of rawseafood and leads to severe abdominal pain(Sugimachi et al. 1985). The tissue damage bythe larvae causes intestinal anisakiosis. Furtherchanges include invasion of the gut wall, andeosinophilic granuloma, or perforation whichmay lead to symptoms such as fever, abdominalpain, vomition and bloody stools.

5.3.7 Clinical Signs in Animals

The parasite larvae may lead to liver atrophy,perforations of the stomach wall, visceral adhe-sions and muscle damage (Smith and Wootten1978). In marine mammals, parasites have beenfound embedded in gastric mucosa tumours(Acha and Szyfres 2006).

5.3 Anisakiosis 87

5.3.8 Diagnosis

The disease can be diagnosed by upper gastro-intestinal endoscopy for visualisation of theworm (McCarthy and Moore 2000) or usingmolecular techniques (Mattiucci et al. 2011).

5.3.9 Control

Prevention and control measures include healtheducation; avoid eating raw or undercookedfish and heating or freezing of fish at appro-priate time–temperature combinations beforeconsumption.

5.4 Ascariosis

Order: AscarididaSuperfamily: Ascaridoidea

5.4.1 Common Name/Synonyms

Ascaridiasis

5.4.2 Etiology

Ascariosis occurs due to Ascaris lumbricoidesand Ascaris suum; two closely related speciesresponsible for the disease in humans and pigs,respectively (Dold and Holland 2010). Thesespecies are morphologically indistinguishablewith few molecular variations (Anderson et al.1993). Albeit both the parasites are specific totheir hosts (Crompton 2001), experimentalstudies have shown that they can infect both thehosts (Takata 1951; Galvin 1968). In personsliving in low prevalence areas of human para-sites, A. suum could cause zoonotic infections(Crewe and Smith 1971; Jaskoski 1961; Lordand Bullock 1982; Nejsum et al. 2005). Theparasite A. suum has also been found among zoochimpanzees (Nejsum et al. 2010).

Fig. 5.2 Life cycle of Anisakis, Pseudoterranova, or Contracaecum species

88 5 Nematode Zoonoses

5.4.3 Epidemiology

A. lumbricoides is a common human parasiteworldwide and more than 1.2 billion people arebelieved to be infected globally (de Silva et al.2003). A. lumbricoides has been commonlyreported from sub-Saharan Africa, Americas,China and East Asia (WHO 2006). A. suum isanother parasite prevalent across the globeand infects pigs with high prevalence rates(Roepstorff et at. 1998; Nansen and Roepstorff1999). Zoonotic ascariosis due to A. suum hasbeen reported in North America, Denmark(Anderson 1995; Nejsum et al. 2005) andthe United Kingdom (Nejsum et al. 2010).Chimpanzees in the Copenhagen Zoo werefound infected with A. suum from pigs bymolecular analysis (Nejsum et al. 2005).

5.4.4 Transmission

Human beings become infected after accidentalingestion of Ascaris eggs through contaminatedfood, water or soil.

5.4.5 Life Cycle

The disease is transmitted via faecal-oral route.After ingestion of infective eggs, L3 larvaehatches in the intestine (Geenen et al. 1999).This is followed by movement of larvae fromsmall to large intestine and further penetration ofthe mucosa (Murrell et al. 1997). Later, thelarvae reach the liver via blood circulation andshed L2 cuticle and finally migrates to the lungs(Roepstorff et al. 1997). The larvae penetratealveolar space and move towards pharynx wherethey are swallowed. The larvae again return tosmall intestine where they mature and reachsexual maturity (Pilitt et al. 1981; Roepstorffet al. 1997). The eggs are shed in faeces anddevelop to infective larvae under favourableconditions.

5.4.6 Clinical Signs in Manand Animals

Clinical symptoms may range from asymptom-atic to severe coughing and wheezing. The lowerage groups are usually affected. Ascaris pnu-monia could result due to damage caused bylarvae. Heavy worm loads may lead to intestinalblockage and obstruction in children. Furthercomplications include intussusception, perfora-tion and gangrene of the bowel. In endemicareas, biliary and pancreatic disease could leadto biliary colic, acute cholecystitis, acute cho-langitis, acute pancreatitis and hepatic abscess.

5.4.7 Diagnosis

The disease can be diagnosed by detection of theparasitic eggs during the intestinal phase of thedisease. Clinical signs such as laboured breath-ing, stunting etc. can also aid in the diagnosis.Serological, molecular (Zhu et al. 1999) tech-niques can provide some help during themigratory phase of the larvae.

5.4.8 Control

Prevention and control measures includeimproved personnel hygiene, health education,improved sanitary measures and chemotherapy(Hotez et al. 2006).

5.5 Baylisascariasis

Order: AscarididaSuperfamily: Ascaridoidea

5.5.1 Etiology

The disease occurs due to Baylisascaris procy-onis, the intestinal roundworm of raccoons,

5.4 Ascariosis 89

which has been regarded as a cause of severeneurologic disease among humans (Sorvilloet al. 2002) since last 2–3 decades.

5.5.2 Epidemiology

This parasite is found in raccoons from NorthAmerica and has also been recorded in othercountries from Europe and Asia (Snyder 1987;Wirtz 1982). Fourteen confirmed human casesdue to B. procyonis have been cited in the lit-erature (Wise et al. 2005; Gavin et al. 2005).

5.5.3 Transmission

Human beings become infected after ingestionof infective eggs from environment contami-nated with racoon faeces.

5.5.4 Life Cycle

The North American raccoon (Procyon lotor)acts as the definitive host for B. procyonis.Intermediate hosts include small birds andmammals (particularly rodents). Humans act asaccidental intermediate hosts. The importantrisks for human infection include young childrenwith pica or geophagia (Kazacos 2000). Rac-coons become infected with B. procyonis throughtwo ways: either through ingestion of infectiveeggs from contaminated environment or afterconsumption of paratenic hosts (Wise et al. 2005;Kazacos 2001). The larvae are released betweeneggs and they develop into male and female adultworms (Kazacos 2001). Gravid females againstart releasing eggs into the faeces. The eggsundergo embryonation and become infective(Kazacos 2001). The paratenic hosts such assquirrels and rodents play an important role in thecompletion of the life cycle. After they ingesteggs, larvae are released which penetrate anddisseminate in different organs and tissues. Lar-vae often migrate to the central nervous system(CNS) (Tiner 1953) and these paratenic hosts are

consumed by racoons. The larvae mature inracoon to become male and female adults andshed eggs (Kazacos 1983, 2001) (Fig. 5.3).

5.5.5 Clinical Signs in Man

B. procyonis could rarely lead to fatal or neuro-logically devastating neural larva migrans(NLM). This results in acute eosinophilicmeningoencephalitis in infants and young chil-dren (Goldberg et al. 1993; Kazacos et al. 1985;Gavin et al. 2005). Pica, exposure to infectedraccoons and contaminated environments withracoon faeces are the three significant risk factorsfor infection (Gavin et al. 2005). The parasitemay occasionally lead to ocular larva migrans(OLM) usually in healthy adults. Clinical symp-toms are not fully understood but could includevisceral, neural and ocular larva migrans.

5.5.6 Clinical Signs in Animals

The infection in raccoons is generally subclini-cal. B. procyonis is considered as the mostcommon cause of clinical larva migrans in someother animals such as rodents, particularly NLM(Gavin et al. 2005). The case reports of infectionin dogs and cats have also been reported(Kazacos 2001; Greve and O’Brien 1989;Averbeck et al. 1995).

5.5.7 Diagnosis

The disease can be diagnosed from clinical signsand history, brain biopsy or serological tests andidentification of ellipsoidal and dark brownB. procyonis eggs (Kazacos 2001).

5.5.8 Control

Avoid contact with raccoons or their faeces andpractice good sanitary measures.

90 5 Nematode Zoonoses

5.6 Capillariasis

Superfamily: TrichuroideaFamily: Capillariidae

5.6.1 Etiology

The nematodes Capillaria hepatica, C. aerophilaand C. philippinensis are responsible for hepatic,pulmonary and intestinal capillariasis in man(Cross 1992). Out of these, C. philippinensisrelated intestinal capillariasis is most importantdisease in human beings.

5.6.2 Epidemiology

Epidemics due to C. philippinensis have beenreported from Philippine islands, Thailand andTaiwan (Cross 1992). In Philippines and Thai-land, more than 2,000 cases have been reported.

Sporadic cases have also been reported frommany other countries such as Korea, Japan,Taiwan, India, Iran, Egypt, Italy, United ArabEmirates, Spain and United Kingdom (Cross1998; El Hassan and Mikhail 1992; Austin et al.1999). Increasing number of cases of Intestinalcapillariasis are being reported from Asia (Hongand Cross 2005).

5.6.3 Reservoir

Fish-eating birds act as the reservoir hosts(Cross 1998) for intestinal capillariasis. Rodentsserve as reservoir for C. hepatica infections.

5.6.4 Transmission

Human beings become infected after consump-tion of tiny freshwater and brackish-water fish(Cross 1998).

Fig. 5.3 Life cycle of Baylisascaris procyonis

5.6 Capillariasis 91

5.6.5 Life Cycle

For C. philippinensis, fish act as intermediatehost and fish-eating birds or man are the defin-itive host for intestinal capillariasis (Bhaibulayaand Indra-Ngarm 1979; Cross and Basaca-Sevilla 1983). Human beings become infectedafter accidental consumption of the tiny fishwhich are normally consumed by birds.

5.6.6 Clinical Signs in Man

The symptoms of intestinal capillariasis includesevere enteropathy and abdominal pain, intermit-tent diarrhoea, weight loss and occasionally deathinhuman beings (Cross 1992,1998) if the cases arenot properly treated. Hepatic capillariasis couldresult in hepatomegaly, abdominal discomfort,diarrhoea, constipation etc. C. aerophila causespulmonary capillariasis and related symptoms.

5.6.7 Clinical Signs in Animals

C. hepatica capillariasis and C. aerophilacapillariasis can cause clinical disease in rodentsand foxes, respectively.

5.6.8 Diagnosis

The disease can be diagnosed by stool examina-tion. Capillaria spp. eggs should be differentiatedfromothercloselyrelatedspeciessuchasTrichurisand Trichinella. If eggs, larvae or adult ofC. philippinensis are not found in the stool sam-ples, biopsy specimens could help in the diagnosis.

5.6.9 Control

Avoid eating raw or undercooked fish in ende-mic areas.

5.7 Cutaneous Larva Migrans

Superfamily: Ancylostomatoidea

5.7.1 Common Name/Synonyms

Creeping eruption, serpiginous eruption, larvacurrens (Strongyloides spp. infection)

5.7.2 Etiology

Cutaneous larva migrans (CLM) occurs due tosubcutaneous migration of the nematode larvae,especially animal hookworms. The etiologicalagents include Ancylostoma braziliense, Ancy-lostoma caninum, Ancylostoma ceylanicum,A. tubaeforme, Uncinaria stenocephala orBunostomum phlebotomum. A. braziliense ismostly responsible for the occurrence of diseasein human beings (Caumes 2000). Many otherparasites such as Strongyloides papillosus,S. westeri, S. stercoralis, S. procyonis andS. myopotami can occasionally cause a similardisease but they move more rapidly than animalhookworms. Moving Gnathostoma spinigerumand Dirofilaria repens could also cause a similartype of dermatitis.

5.7.3 Epidemiology

A. braziliense is endemic in tropical and sub-tropical areas, whereas A. caninum and B. phle-botomum more commonly occur in temperateareas. Human cases have been reported acrossthe globe from many countries (Shinkar et al.2005; Yoshida et al. 1973). Travellers visitingendemic areas are at particular risk of theinfection.

92 5 Nematode Zoonoses

5.7.4 Reservoir

Carnivorous animals act as reservoir for theinfection.

5.7.5 Transmission

Human beings become infected due to penetra-tion of the parasite larvae present in the soilcontaminated by infected animal faeces.

5.7.6 Life Cycle

In carnivorous animals, the larvae present in thesoil penetrate the skin and migrate through thetissue to reach small intestine of the host wherethey mature into adults. In human beings, althoughlarva penetrates and migrates through skin, but itdo not develop further and cause the disease.

5.7.7 Clinical Signs in Man

These migrating larvae produce erythematous,serpiginous, pruritic, cutaneous track also knownas creeping eruption (Caumes et al. 2002;Beaver 1956; Bryceson and Hay 1998; Lucchinaand Wilson 1999) due to percutaneous penetra-tion and subsequent migration of larvae of manynematode parasites (Knight 2003).

5.7.8 Clinical Signs in Animals

The disease occurs in carnivorous (dogs and cat)animals. The symptoms include diarrhoea,anaemia and allergic dermatitis.

5.7.9 Diagnosis

The disease can be diagnosed by clinicalsymptoms, successful treatment or by histopa-thological confirmation (Purdy et al. 2011).

5.7.10 Control

For prevention and control, one should not walkbarefoot and use a mattress while lying in sandyareas particularly in disease endemic tropicaland subtropical areas.

5.8 Dioctophymosis

Superfamily: DioctophymatoideaFamily: Dioctophymidae

5.8.1 Common Name/Synonyms

Dioctophymiasis

5.8.2 Etiology

Dioctophymosis occurs due to Dioctophymarenale, a large nematode also known as the giantkidney worm (Soulsby 1978; Bowman 1999).

5.8.3 Epidemiology

The parasite has been reported across the globebarring Africa and Oceania (Soulsby 1978;Freitas 1980; Kommers et al. 1999). The parasitebasically infects domestic and wild fish-eatingcarnivores (Soulsby 1978; Maxie 1993;Bowman 1999; Nakagawa et al. 2007) but hasthe ability to cause the disease in human beings(Sun et al. 1986; Acha and Szyfres 2006).Among domestic animals, the parasite is morecommonly found in dogs than cats, horses andcattle (Maxie 1993; Nakagawa et al. 2007). Theadult parasite is usually found in kidney but canalso occur in abdominal cavity, uterus, ovary,mammary gland, urethra, subcutaneous tissuesof the inguinal region and mesenteric lymphnodes (Freitas 1980; Maxie 1993).

5.7 Cutaneous Larva Migrans 93

5.8.4 Reservoir

The mink (Mustela vison) is considered to be themain reservoir and definite host (Bowman1999), and humans and dogs are thought to beterminal or accidental hosts (Acha and Szyfres2006; Nakagawa et al. 2007).

5.8.5 Transmission

Human beings become infected after eatinginfected raw fish, frogs or by drinking watercontaminated with the mud-worm infected byD. renale in its larval form.

5.8.6 Life Cycle

The life cycle of the parasite involves differentkind of hosts (Soulsby 1978; Freitas 1980;Bowman 1999). The eggs of the parasite arepassed in the urine and are ingested by interme-diate hosts viz. mud-worms (aquatic oligochae-tes). The nematode develop into third stage larva(Freitas 1980) in mud worms and then these areeaten by fishes or frogs which act as paratenichosts and the larvae become ingested in tissuewithout further development (Bowman 1999).Wild fish eating carnivores act as the definite hostsand become infected after consuming infectedintermediate or paratenic host (Soulsby 1978;Bowman 1999). The larva migrates to the kidneyin the definitive host (Freitas 1980; Bowman1999; Nakagawa et al. 2007).

5.8.7 Clinical Signs in Animals

In dogs, most cases generally remain asymp-tomatic (Soulsby 1978; Maxie 1993) or theclinical signs are not conclusive for the defini-tive diagnosis of the disease. Right kidney andabdominal cavity are more commonly affectedin case of dogs (Freitas 1980; Maxie 1993;

Bowman 1999; Kommers et al. 1999). Theinfection could lead to renal parenchyma atro-phy, dilation of the renal pelvis and urethralobstruction (Soulsby 1978; Maxie 1993). Othersigns such as renal failure, haematuria, abdom-inal distention and peritonitis may also beobserved.

5.8.8 Clinical Signs in Man

The parasitic infection could lead to similar kindof symptoms in man.

5.8.9 Diagnosis

The disease can be diagnosed using imagingtechniques such as radiology (Nakagawa et al.2007), sonography (Soler et al. 2008) anddetection of parasite ova or eggs (Birchard andSherding 1994) in the urine. Postmortem-baseddetection of the parasite is another method rou-tinely employed for detection of the parasite(Pereira et al. 2006).

5.8.10 Control

Avoid consumption of raw or undercooked fishand frog or water contaminated with infectedmud worms.

5.9 Dracunculiasis

Class: SecerenteaSuborder: CamallinidaSuperfamily: Dracunculoidea

5.9.1 Common Name/Synonyms

Guinea worm disease, Dracontiasis

94 5 Nematode Zoonoses

5.9.2 Etiology

The disease occurs due to guinea wormDracunculus medinensis, one of the longest tis-sue nematode which can infect human beings.

5.9.3 Epidemiology

The parasite was prevalent in southern Asia andNorth, West and East Africa for past two dec-ades (Tiben and Hopkins 2006). After the end of2007, the disease remains endemic only in fewcountries viz. Sudan, Ghana, Mali and Niger dueto successful implementation of dracunculiasiseradication programme (Hopkins et al. 2008).

5.9.4 Reservoir

Human being acts as the reservoir ofD. medinensis.

5.9.5 Transmission

Human beings become infected after drinkingwater from stagnant ponds, pools, cisterns oropen wells containing fresh water copepods(Cyclops or water fleas) harbouring infectivelarvae of the parasite (Tiben and Hopkins 2006).

5.9.6 Life Cycle

The first stage larvae are released by femaleworm when they emerge from the human body.The released larvae remain in the water and areingested by an intermediate host, copepod.Larvae develop into third stage in the copepod(Cairncross et al. 2002; Muller 1971). Humanbeings become infected after drinking watercontaining infected copepods. In human beings,gastric juices digest the vector and release larva.The larvae migrate through thoracic cavity and

enter connective tissues to reach maturity. Mat-ing occurs, female continue their developmentand emerge from lower part of the human body(Karam and Tayeh 2006). Blister formationoccurs and female worm releases thousands oflarvae after contact with cold water (Muller1971) (Fig. 5.4).

5.9.7 Clinical Signs in Man

In human beings, the symptoms start with theformation of cutaneous blister. There is intenseburning sensation and symptoms could extend toerythema, urticarial rash, intense pruritus, nau-sea and vomiting, diarrhoea, dyspnoea, giddi-ness and syncope (Muller 1971). After the blisterbursts, symptoms start to disappear slowly. If thelarvae are released inside the joint, it may lead tosevere arthritis and ankylose.

5.9.8 Clinical Signs in Animals

Clinical manifestations are similar as in man.Few presumed zoonotic cases have been reportedin Japan, Korea and Indonesia, where disease isnot endemic and these infections might haveoccurred from animal reservoirs (Hashikura1927; Kobayashi et al. 1986; Van Heutsz 1926).Possibly, the infection occurred after consump-tion of raw freshwater fishes as paratenic hosts(Cairncross et al. 2002). Emerging female wormshave also been recovered occasionally from awide range of mammals from both endemic andnon-endemic areas (Cairncross et al. 2002).

5.9.9 Diagnosis

The disease can be diagnosed from the clinicaland allergic symptoms or using immunodiag-nostic/serological tests (Bloch et al. 1993, 1998;Bapna and Renapurkar 1996).

5.9 Dracunculiasis 95

5.9.10 Control

The ponds and shallow or step wells are theimportant sources of the disease. The provisionof clean drinking water is a must for preventionand control of the disease.

5.10 Gnathostomiasis

Superfamily: SpiruroideaFamily: Gnathostomatidae

5.10.1 Common Name/Synonyms

Gnathostomiasis, larva migrans (Gnathostoma)

5.10.2 Etiology

Gnathostomiasis is important food-borne zoono-sis of public health significance. The diseaseoccurs due to 12 species of Gnathostoma(Guitierrez2000;HermanandChiodini2009).Outof these, 4 species have been recorded in humanbeings viz. G. spinigerum (reported from wild anddomestic cats and dogs in India, China, Japan andsoutheast Asia), G. hispidum (reported from wild

and domestic pigs in Europe, Asia and Australia),G. doloresi (reported from wild boars) andG. nipponicum (reported from weasels in Japan)(Guitierrez 2000; Herman and Chiodini 2009).

5.10.3 Epidemiology

The disease is endemic in Japan, Thailand andparts of Southeast Asia (Rusnak and Lucey 1993).The disease has also been reported from Centraland South America, Cambodia, Laos, Myanmar,Indonesia, Philippines, Malaysia, China, SriLanka and India (Rusnak and Lucey 1993).

5.10.4 Reservoir

In endemic areas, cats, dogs and pigs can serveas important reservoirs of infection (Daensvang1980; Moore et al. 2003),

5.10.5 Transmission

Human beings become infected after consump-tion of raw or undercooked infected freshwaterfish or snakes, frogs, chickens and pigs. Inges-tion of water containing infected copepod

Fig. 5.4 Life cycle of Dracunculus medinensis

96 5 Nematode Zoonoses

is another important risk for the infection(Daengsvang 1981).

5.10.6 Life Cycle

The adult parasites live in the stomach wall of fishconsuming carnivores and shed the eggs in theirfaeces. When eggs are shed in freshwater, firststage swimming larvae form which are consumedby first intermediate host small crustaceancyclops. Fish consume these hosts and infectivelarvae develop in fish muscle tissue as L3 larvae. Indefinitive host, adult parasite develops after con-sumption of infected fish. For G. spinigerum, feralcats and dogs mainly act as definitive host, butinfections have also been recorded from tigers,leopards, lions, racoons, minks, opossums andotters (McCarthyandMoore2000).Human beingsaccidentally become infected after consumptionof infected fish. Additionally, pigs, frogs, snails,chickens and snakes can also act as intermediatehosts (McCarthy and Moore 2000) (Fig. 5.5).

5.10.7 Clinical Signs in Man

The symptoms include malaise, fever, urticaria,anorexia, nausea, vomition, diarrhoea, and epi-gastric pain (Rusnak and Lucey 1993). Theparasite migrates through skin and subcutaneoustissue leading to painful swelling and cutaneousgnathostomiasis (Rusnak and Lucey 1993).Occasionally, parasite may migrate to othervisceral organs and could lead to pulmonary,ocular, genitourinary, gastrointestinal, auditoryand central nervous gnathostomiasis with fatalconsequences (Rusnak and Lucey 1993).

5.10.8 Clinical Signs in Animals

In their respective definitive hosts, the parasiteproduces clinical symptoms. Necrotic tunnels invisceral organs (such as liver, pancreas),abdominal tissues and peritonitis can occur incat and dogs due to G. spinigerum infections

(Acha and Szyfres 2006). Stomach ulcers andother abdominal symptoms could also be seen inpigs infected with G. hispidum and G. doloresi(Acha and Szyfres 2006).

5.10.9 Diagnosis

Clinical signs, history and serological tests canhelp in diagnosis of the disease.

5.10.10 Control

Avoid eating raw or undercooked intermediatehosts such as fish, snakes, frogs, chicken etc. anddrink clean water. Freezing of meat to -20 �Cfor 3 to 5 days can also render meat safe forconsumption (Herman and Chiodini 2009).

5.11 Gongylonemosis

Order: SpiruridaSuperfamily: SpiruroideaFamily: Thelaziidae

5.11.1 Common Name/Synonyms

Gongylonematosis

5.11.2 Etiology

The disease primarily occurs due to Gongylo-nema pulchrum, Molin 1857, a spiuroid nema-tode although many other species ofGongylonema, could also affect mammals andbirds (Soulsby 1982; Yamaguti 1961; Cappucciet al. 1982). Ruminants, pigs and wild boar arethe main definitive hosts of this parasite, but ithas also been reported from nonhuman primates,carnivores and rodents. Human beings becomeaccidentally infected after ingestion of interme-diate host or drinking contaminated water.

5.10 Gnathostomiasis 97

5.11.3 Epidemiology

Although a rare zoonosis, but the disease inhumans is wide in distribution. More than 50human cases have been reported from China,Middle East, Australia, Italy, United States,Europe, Sri Lanka, New Zealand, Japan andSoutheast Asia (Wilde et al. 2001; Cappucciet al. 1982).

5.11.4 Reservoir

Existence of large number of definitive andintermediate hosts serves as source of infection.

5.11.5 Transmission

Accidental ingestion of small beetles possiblythrough contaminated salad and vegetablescould serve as source of infection in man.

5.11.6 Life Cycle

Approximately fifty species of arthropodcoprophagous insects such as dung beetles,cockroaches, etc. act as intermediate hosts forG.pulchrum (Cappucci et al. 1982; Illescas-Gomez et al. 1988; Soulsby 1965). Embryo-nated eggs are shed in the faeces of definitive

Fig. 5.5 Life cycle of Gnathostoma spinigerum

98 5 Nematode Zoonoses

host and they are further consumed by inter-mediate hosts. The third stage larva develops inthe intermediate host. Definitive hosts becomeinfected after ingestion of these intermediatehosts, whereas swine mostly become infecteddue to coprophagia (Wilde et al. 2001;Cappucci et al. 1982).

5.11.7 Clinical Signs in Man

In human beings, sensation occurs due to themovements of the worm. The parasite can pro-duce irritation in buccal mucosa, and occasion-ally may cause bloody expectoration, tarrystools, numbness of tongue, pain in chest andabdomen, vomiting, bloating, pharyngitis andstomatitis (Cappucci et al. 1982; Kudo et al.2008). Association between oesophageal squa-mous cell carcinoma and gongylonemosis hasalso been reported (Bleier et al. 2005).

5.11.8 Clinical Signs in Animals

In animals, the lesions include mild or chronicinflammatory changes in the affected parts. Theinfection may also lead to occlusions of theoesophagus due to reflex action produced byirritation.

5.11.9 Diagnosis

The disease can be diagnosed by history ofmoving worm followed by further parasiteidentifications.

5.11.10 Control

Improved personnel and environmental hygienecan help to prevent the disease.

5.12 Lagochilascariosis

Order: AscarididaSuperfamily: Ascaridoidea

5.12.1 Etiology

There are five species of genus Lagochilascaris:L. minor, L. major, L. buckleyi, L. turgida andL. sprenti (Leiper 1909; Sprent 1971). The humandisease occurs due to the nematode L. minor (Pacoet al. 1999).

5.12.2 Epidemiology

L. minor lagochilascariosis is present in Neo-tropical areas (from Mexico to Brazil), Uruguay(Sakamoto and Cabrera 2002). It is an emergingzoonotic disease in Brazil (Fraiha et al. 1989;Barbosa et al. 2006; Prudente et al. 2008; Freire-Filha et al. 2001). Rural and low socioeconomicstatus populations are at the high risk of infec-tion in endemic areas.

5.12.3 Reservoir and Transmissionof the Disease

Natural reservoirs and transmission of the dis-ease are not clear. Ingestion of embryonatedeggs released by another species might be thecause of disease in man.

5.12.4 Life Cycle

Albeit, the life cycle is not fully understood,but there is strong belief that cats act as thedefinitive host for this parasite. The adultworms are present in the upper portion of the

5.11 Gongylonemosis 99

respiratory or digestive tract and eggs are pas-sed through faeces of the cat. Synanthropic ratsand other rodents ingest the infective eggscontaining third stage larvae and act as theintermediate hosts for this parasite. Further,larvae hatch in the intermediate host andmigrate to different organs such as liver, lungsand form cysts in the muscle and subcutaneoustissue (deMoura et al. 2012; Campos et al.1992; Volcan et al. 1992). Humans and thecanids, act as accidental hosts after consump-tion of raw or undercooked infected rodentmeat (Campos et al. 1992). Rodents (Paco et al.1999) capybara (Hidrochaeris hidrochaeris)and agouti (Dasyprocta aguti) are particularlyimportant. The developmental stages could befound in cat or other accidental definitive hosts(Leão et al. 2005).

5.12.5 Disease in Man

Important clinical signs in humans include puru-lent subcutaneous tissue abscess in ear, neck, jaw,orbit, mastoid process, head and presence of eggs,larval and adult parasites in retropharyngeal tissue(Leiper 1909; Olle-Goig et al. 1996; Moncadaet al. 1998). In rare cases, the parasite may affectpulmonary tissue or central nervous system(Rosemberg et al. 1986; Veloso et al. 1992)leading to death (Sakamoto and Cabrera 2002).

5.12.6 Disease in Animals

The symptoms in the definitive host are notmuch clear. Two reported cases in cat revealedpresence of fistulated abscesses (deFreitas et al.2008; Amato et al. 1990).

5.12.7 Diagnosis

The disease can be diagnosed by identificationof eggs in the faeces or from identification of theparasite in affected lesions.

5.12.8 Control

No specific control measures are known for thisdisease.

5.13 Mammomonogamus

Order: StrongylidaSuperfamily: StrongyloideaFamily: Syngamidae

5.13.1 Common Name/Synonyms

Syngamiasis

5.13.2 Etiology

The disease occurs due to Mammomonogamuslaryngeus (Syngamus laryngeus). This parasiteis generally present in laryngotracheal region ofcattle and some other bovines (Gutierrez 1999;Anderson et al. 1980). The other parasiteM. nasicola is present in nasal fossa of bovids.These parasites are found in the larynx of cattle(Anderson et al. 1980) and are found rarely inhuman beings (Beaver et al. 1984).

5.13.3 Epidemiology

More than 100 human infections due toM. larygeus (Gutierrez 1999; Nosanchuk et al.1995; da Costa et al. 2005; Angheben et al.2009) have been reported from different coun-tries such as Caribbean Islands, South America(especially Brazil), Australia, Canada, the Uni-ted States, France, United Kingdom (Cunnacet al. 1988), Philippines (Beaver et al. 1984),Thailand (Pipitogool et al. 1992), Italy (Anghe-ben et al. 2009) and Korea (Kim et al. 1998).The parasite is mainly found in the Caribbeanand South America and other cases have beenreported from tourists visiting these areas(da Costa et al. 2005).

100 5 Nematode Zoonoses

5.13.4 Reservoir

Ruminants act as reservoirs for M. laryngeus andM. nasicola.

5.13.5 Transmission

The transmission cycle of the parasite is notclearly known. It is thought that infection occurseither after ingestion of embryonated egg, hat-ched larvae or paratenic host such as earth-worms, snails, or arthropods. Contaminated rawvegetables or drinking water could also serve asa source of infection.

5.13.6 Life Cycle

Life cycle of the parasite is not fully understoodbut it is assumed that it penetrates the intestinalwall and then migrates to the tracheolaryngealregion through the body (Gutierrez 1999; Severoet al. 1988). The eggs are produced by theparasite in the tracheal mucosa, which areswallowed and are then passed through thefaeces.

5.13.7 Clinical Signs in Man

The symptoms primarily include chronic cough,fever and occasionally hemoptysis. Addition-ally, parasite may cause irritation of the larynxand asthma.

5.13.8 Clinical Signs in Animals

The disease is not symptomatic in animals.Ruminant infections have been recorded fromtropical America, Africa, India, Malaysia, Viet-nam and Philippines (Acha and Szyfres 2003).

5.13.9 Diagnosis

The disease can be diagnosed by brochoscopicor expectorated identification of the parasite(Gutierrez 1999). Eggs may also be seen insputum or faeces of infected persons.

5.13.10 Control

Improved personnel hygiene can help preventinfection in human beings.

5.14 Micronemosis

Order: RhabditidaSuperfamily: Rhabditoidea

5.14.1 Etiology

The disease occurs due to Micronema deletrix(Synonym: Halicephalobus gingivalis), a smallfree living nematode. The parasite is mostcommonly found in brain but could be found inkidneys, oral and nasal cavities, lymph nodes,spinal cord and adrenal glands (Spalding et al.1990; Rames et al. 1995).

5.14.2 Epidemiology

Micronemosis has been reported from UnitedStates (Anderson and Bemrick 1965; Rubin andWoodard 1974; Alstad et al. 1979; Simpsonet al. 1988), Switzerland (Pohlenz et al. 1981)and Netherlands (Keg et al. 1984) in horses.

5.14.3 Reservoir

This parasite is found in close association withdecaying humus (Anderson and Bemrick 1965;

5.13 Mammomonogamus 101

Poinar 1983). The opportunistic parasitedepends for food on bacteria, but may becomeindependent for its development (Poinar 1983).

5.14.4 Transmission

The route of transmission is not fully understoodbut it is believed to be through contamination oforal or nasal wounds, due to common parasiteinfestation of these sites. The manure contami-nation of cutaneous lacerations or decubitalulcers was also found responsible for two humancases with CNS involvement (Gardiner et al.1981; Rames et al. 1995).

5.14.5 Life Cycle

M. deletrix is a facultative parasite of man andanimals as all the developmental stages havebeen found in the environment outside the bodyof human and animal hosts (Shadduck et al.1979; Acha and Szyfres 2003).

5.14.6 Clinical Signs in Man

In humans, three cases of M. deletrix microne-mosis responsible for parasitic meningoenceph-alitis have been recorded in Canada (Hoogstratenand Young 1975) and the United States(Shadduck et al. 1979; Gardiner et al. 1981).

5.14.7 Clinical Signs in Animals

Among horses, the parasite was found to causeinfection in nasal passages, lung, lymph nodes,stomach, maxillae, mandible, brain, kidney,adrenal glands and femur (Gordon et al. 1990).

5.14.8 Diagnosis

The diagnosis can be done at the time of post-mortem using histological examination of theaffected organs.

5.14.9 Control

Improved personnel hygiene can help preventinfection in human beings.

5.15 Oesophagostomiasis

Order: StrongylidaSuperfamily: StrongyloideaFamily: Trichonematidae

5.15.1 Common Name/Synonyms

Esophagostomiasis, Ternidensiasis

5.15.2 Etiology

Oesophagostomiasis occurs due to strongylidintestinal parasites Oesophagostomum bifurcum,O. stephanostomum, O. aculeatum and Terni-dens derminutus of non-human primates andhumans (Remfry 1978; McCarthy and Moore2000). Out of these, O. bifurcum was considereda rare zoonosis. The zoonotic potential ofO. bifurcum is still not fully understood. Recently,epidemiological, molecular and morphologicalstudies on O. bifurcum from humans and variousmonkeys clarified that different strains ofO. bifurcum are prevalent in humans and monkeysand they are specific to their respective hostsindicating a non-zoonotic transmission betweenthese species (Polderman et al. 2010). However,another study carried out in western Ugandaindicates that O. bifurcum are prevalent in chim-panzees which have potential for zoonotic trans-mission of these species (Krief et al. 2010).

5.15.3 Epidemiology

O. bifurcum is widely prevalent in West Africa,but a few cases have also been reported fromother parts of Africa, Asia and South America(Bogers et al. 2001).

102 5 Nematode Zoonoses

5.15.4 Reservoir

Non-human primates are thought to be theimportant reservoir hosts.

5.15.5 Transmission

Humans become infected after ingestion ofinfective larvae from soil contaminated withfaeces of non-human primates.

5.15.6 Life Cycle

Humans or primates become infected afteringestion of L3 larvae. The larvae penetratecolon and some of these larvae develop andreturn to the bowel lumen, while others becomeimmature worms and lead to formation ofabscess in the bowl lumen. Adult mature wormsmate and shed eggs in the faeces. The eggs hatchin soil and develop from L1 to L3 infectivelarvae (Polderman and Blotkamp 1995).

5.15.7 Clinical Signs in Manand Animals

Most of the times, infections are not symptom-atic. Two forms of the disease viz. multinodularand uninodular (Dapaong tumour) can occur(Polderman and Blotkamp 1995). Clinical signsinclude ‘Dapaong tumour’, named after thecapital of Togo’s northernmost province. In thisan inflammatory mass develop around juvenileworms in the colonic wall or abdominal cavity.Adhesions develop around the abdominal walland this may lead to occasional obstruction ofcolon (Storey et al. 2000; Polderman et al.1999). Heavy infections can lead to diarrhoea,weight loss, weakness and death in man.

5.15.8 Diagnosis

The disease can be diagnosed after parasiticidentification and stool culture on stool charcoalmixture (Polderman et al. 1991), PCR–RFLPand Random Amplified Polymorphic DNA—Gel—electrophoresis.

5.15.9 Control

Improved personnel hygiene, chemotherapy ofinfected animals can help control the infection.

5.16 Strongyloidiasis

Order: RhabditidaSuperfamily: RhabditoideaFamily: Strongyloididae

5.16.1 Common Name/Synonyms

Strongyloidiasis, threadworm infection

5.16.2 Etiology

The disease occurs due to the parasite Strongy-loides stercoralis and S. fuelleborni. Role of theanimal hosts dogs and cats for S. stercoraliszoonotic infections is not clearly understood. It isbelieved that they might be contributing to humaninfections in some parts of the world. The zoo-notic potential of S. fuelleborni is believed to bemuch higher than S. stercoralis. It mainly infectsnon-human primates but can cause zoonotic dis-ease in Africa and Southeast Asia or at least have azoonotic origin (Ashford and Barnish 1989; Olsenet al. 2009). Other Strongyloid infections can alsocause dermatitis in man which can be zoonotic innature.

5.15 Oesophagostomiasis 103

5.16.3 Epidemiology

S. stercoralis infections could be seen across theglobe but is particularly endemic in tropical andsubtropical areas viz. Southeast Asia, sub-SaharanAfrica, Latin America, and the south-easternUnited States (Berk et al. 1987). The parasite isbelieved to be affecting 100–200 million personsworldwide (Genta 1989). S. fullerborni infectionsoccur in non-human primates of Africa and Asia.S. stercoralis infection can occur for very longperiods of time due to the ability of the parasite tocause autoinfection which result in persistentchronic infections (Grove 1996). Poor sanitaryconditions are important factor for S. stercoralisinfections (Hall et al. 1994).

5.16.4 Reservoir

Humans are reservoir for S. stercoralis infec-tions. For S. fuelleborni infections, African andAsian simians serve as important reservoirs.

5.16.5 Transmission

The disease occurs through direct skin contactwith contaminated soil particularly in agricul-tural and recreational activities.

5.16.6 Life Cycle

The parasite has both free-living and parasiticstages. The female parasite present in the smallintestine lays eggs in the intestinal mucosa. Theeggs develop into larvae and are shed in the fae-ces. In suitable environment, larvae develop intoinfective filariform larvae or develop into free-living adults. The sexual reproduction of theparasite occurs in the free-living adult stage (Neva1994). The parasite generally enters the humanbody through cutaneous route, enters the blood-stream and reaches through lungs finally to thegastrointestinal tract (Keiser and Nutman 2004).

5.16.7 Clinical Signs in Man

The infection primarily remains asymptomatic(Grove 1989) but can cause symptoms related tocutaneous (pruritus, urticaria), respiratory(cough, chronic bronchitis) and intestinal(abdominal pain, intermittent or persistent diar-rhoea) systems. However, in immune compro-mised individuals, the parasite can cause afulminant fatal disease (Keiser and Nutman2004) viz. hyperinfection (uncontrolled multi-plication) and dissemination of larvae to all thevisceral organs (Olsen et al. 2009).

5.16.8 Clinical Signs in Animals

The disease in dogs and cats is not long lastingand generally infects young puppies. The symp-toms are self limiting and generally resemble asin healthy human beings. Among non-humanprimates, mild to severe haemorrhagic diarrhoeacould occur particularly in young or weakenedanimals (Acha and Szyfres 2003).

5.16.9 Diagnosis

The parasite can be detected using faecal con-centration or culture techniques (Cheesbrough1987). Immunological tests such as Western blot,ELISA and IFAT can also be used in the diag-nosis (Silva et al. 2003; Rodrigues et al. 2007).

5.16.10 Control

Proper disposal of human faeces, treatment ofinfected persons and using protective measuresin endemic areas can help control the disease.

5.17 Thelaziasis

Order: SpiruridaSuperfamily: SpiruroideaFamily: Thelaziidae

104 5 Nematode Zoonoses

5.17.1 Common Name/Synonyms

Oriental eye-worm, thelaziasis, eye worminfections, conjunctival spirurosis

5.17.2 Etiology

Thelazia callipaeda is a helminth responsible forcausing eye infection in humans and animalssuch as domestic cats and dogs (Otranto andEberhard 2011). T. callipaeda causes insect-borne zoonosis in man. Some other species suchas T. californiensis and T. rhodesii could alsocause the disease.

5.17.3 Epidemiology

Among humans, the parasite is distributed inerstwhile Soviet Union and Asian countries suchas China, Korea, Japan, Indonesia, Thailand,Taiwan and India (Otranto and Eberhard 2011).More than 157 cases have been reported acrossthe globe in addition to 100 cases reported fromJapan (Koyama et al. 2000; Kitano et al. 1996;Singh and Singh 1993). Children and old personare at higher risk of being infected. The parasiteis also widespread in domestic and wild animalsin Asia, Italy, France and Germany (Miyazaki1991; Otranto et al. 2003a; Kosin et al. 1989;Shen et al. 2006; Sohn et al. 2011).

5.17.4 Reservoir

Domestic and wild mammals serve as importantreservoirs of disease.

5.17.5 Transmission

The disease is transmitted by secretophagous flieswhich deposit it in the eye orbit of human beings(Otranto and Traversa 2005) and other animals.

5.17.6 Life Cycle

The secretophagous flies play central role intransmission of this disease. These flies feed onthe lachrymal secretions of man and other infec-ted animals and thus ingest first stage larvae in theprocess. The third stage larva develops in the flyand is deposited back into the orbit of the eye.

5.17.7 Clinical Signs in Man

Clinical signs in man include lachrymation,epiphora, conjunctivitis, keratitis and cornealulcers in severe cases (Anderson 1992).

5.17.8 Clinical Signs in Animals

Domestic dogs, cats and wild carnivores (e.g.foxes, wolves and wild cats) are primarilyaffected (Otranto et al. 2009). Symptoms aregenerally similar as in the human infections.

5.17.9 Diagnosis

The disease can be diagnosed after removal ofthe worm from the eye followed by morpho-logical identification of the parasite (Otrantoet al. 2003b).

5.17.10 Control

Avoidance of eye contact with intermediatehosts can prove beneficial for prevention of thedisease.

5.18 Trichinosis

Order: EnoplidaSuperfamily: TrichuroideaFamilly: Trichinellidae

5.17 Thelaziasis 105

5.18.1 Common Name/Synonyms

Trichinellosis, Trichiniasis, Trichinelliasis

5.18.2 Etiology

The disease occurs due to the parasites of genusTrichinella. At present, two clads are recognised:One that contain species which encapsulate inhost muscle cell (T. spiralis, T. nativa, T. britovi,T. murrelli, T. nelsoni and Trichinella T6, T8, T9and T12) and second that do not encapsulate inhost muscle cell (T. psudospiralis, T. papuae,T. zimbabwensis). All the species present in thefirst clad only infect mammals, whereas in sec-ond clad, T. pseudospiralis infects mammals andbirds; and T. papuae, T. zimbabwensis both infectmammals and reptiles (Gajadhar et al. 2009).

5.18.3 Epidemiology

The parasite causes serious zoonosis and as manyas 11 million people may be infected (Dupouy-Camet 2000). Numerous outbreaks of trichinel-losis have been reported in different parts of theworld (Dupouy-Camet 2000). Trichinella infec-tion has been reported in domestic (mainly pigs)and wild life species of 43 and 66 countries,respectively (Pozio 2007). Trichinellosis is aworldwide prevalent nematode zoonotic diseaseof medical, veterinary and economic significance(Dupouy-Camet 2000). Trichinella is one of themost wide spread parasites infecting people andother mammals across the globe in most climates,except for deserts (Dupouy-Camet 2000).Domestication of pigs some 10,000 years ago inAsia created a permanent reservoir of parasitesfor humans, limited by the use of fire and Mosaiclaws (Dupouy-Camet 2000). Trichinellosis sig-nificantly impact national economies due to rea-sons of public health, socioeconomics and trade(Todd 1989; Roberts and Murrell 1993; Ortega-Pierres et al. 2000). The occurrence of significanttransmission from scavenged animal carcasses

suggests that environmental temperature andhumidity play an important role in the transmis-sion of Trichinella among wild life (Pozio 2000).Environmental contamination with Trichinella-infected meat scraps could lead to infectionamong herbivores, particularly in horses (Pozio2000). Unhygienic slaughtering of food animals,roaming behaviour of stray pigs, lack of struc-tured meat inspection, commonly used garbageand kitchen practices for pigs, free access of dogsand cats to slaughter houses, socioeconomicconditions, culinary habits etc. undoubtedlyenhances perpetuation of the transmission cycle.

5.18.4 Reservoir

Wild boar or other animals are important reser-voirs of infection.c

5.18.5 Transmission

Consumption of raw or undercooked pork orwild boar meat is important source for trans-mission of the disease in man.

5.18.6 Life Cycle

Trichinella spp. can complete its life cycle in asingle host. After ingestion of infected meatcontaining first stage infective larvae, digestionof meat in the stomach releases larva whichmature in small intestine in few days (Gajadharet al. 2006) (Fig. 5.6).

The adult female starts shedding larvae. Thelarvae enter blood circulation and reach skeletalmuscles and encapsulate and usually live therefor 3–5 years or more (Gajadhar et al. 2006).The infected meat when consumed by anotherhost restarts the life cycle of the parasite. Highnumbers of Trichinella larvae are present indiaphragm, tongue and massetar muscles(Gajadhar et al. 2006).

106 5 Nematode Zoonoses

5.18.7 Clinical Signs in Man

The number of larvae present, genotype involvedand host immunity determine the severity of dis-ease in man. Clinical signs vary from asymp-tomatic infections to diarrhoea, gastrointestinaldisturbances, periorbital and facial oedema,myalgia, fever, conjunctivitis, headache and skinrash (Gajadhar et al. 2006). In extreme cases, lifethreatening encephalitis, endocarditis, myocar-ditis may also be seen (Gajadhar et al. 2006).

5.18.8 Clinical Signs in Animals

The disease is generally asymptomatic in animals.Among animals, pigs, bear, canids, rodents, skunks,raccoon, walrus, opossum and seals can act as hosts.

5.18.9 Diagnosis

The disease can be diagnosed using trichinos-copy, Trichinella artificial digestion assay,serological, histological, bioassay and moleculartechniques. The digestion assay is more reliableand recommended test to trichinoscopy(Figs. 5.7, 5.8).

5.18.10 Control

Proper meat inspection practices, rodent control,avoiding garbage feeding to pigs, proper carcassdisposal can help control the disease.Consumption of properly cooked meat can avoidinfection in man (Gajadhar et al. 2006).

Fig. 5.6 Life cycle of Tichinella spiralis

5.18 Trichinosis 107

5.19 Trichostrongylosis

Order: StrongylidaSuperfamily: TrichostrongyloideaFamily: Trichostrongylidae

5.19.1 Common Name/Synonyms

Trichostrongyliasis

5.19.2 Etiology

There are several species of the genus which caninfect sheep, goat and bovines. For humaninfections, cases due to Trichostrongylus orien-talis, T. axei, T. colubriformis, T. skrjabini,T. vitrinus, T. probolurus, T. capricola, T. brevis,T. affinis and T. calcaraus have been recorded(Acha and Szyfres 2003).

Fig. 5.7 Numerous coiledinfective Trichinella larvaeseen using trichinelloscopy(with kind permission fromDr. Alvin A Gajadhar,Research Scientist cumHead, Center for Food-Borne and AnimalParasitology, CanadianFood Inspection AgencySaskatoon Lab, Canada)

Fig. 5.8 Coiled infectiveTrichinella larvaerecovered from horse meatusing pepsin HCl digestionassay (with kindpermission from Dr. AlvinA Gajadhar, ResearchScientist cum Head, Centerfor Food-Borne andAnimal Parasitology,Canadian Food InspectionAgency Saskatoon Lab,Canada)

108 5 Nematode Zoonoses

5.19.3 Epidemiology

The disease has been reported across the globe.Sporadic human cases have been reported fromAsian countries such as Thailand, South Korea,China, Laos; United States and Australia (Satoet al. 2011; Beaver et al. 1984; Boreham et al.1995; Panasoponkul et al. 1985; Yong et al.2007; Wall et al. 2011). Farmers and otherpersons involved in dairy farming are at risk ofbeing infected particularly in the developingworld and endemic areas (Adams et al. 2005).Among animals, high prevalence has beenrecorded in Asia and Middle East (Youn 2009;Giboda et al. 1991; Poirriez et al. 1984).

5.19.4 Reservoir

Herbivorous animals act as reservoirs for mostof the Trichostrongylus species.

5.19.5 Transmission

Human beings become infected after consump-tion of contaminated food and water particularlyin the places where animal faeces are used forsoil fertilisation.

5.19.6 Life Cycle

The host species releases eggs in the faeces.These eggs develop into first stage larva. Afterfeeding on organic matter, these larvae furtherdevelop into third stage larva which is infective tothe host. After ingestion of third stage larva, itmature into adult and start releasing eggs in thefaeces of the host.

5.19.7 Clinical Signs in Man

Disease generally remains asymptomatic but inhigh parasitemia, clinical symptoms may includeeosinophilia, bloating diarrhoea, abdominal pain,weight loss and some other abdominal disorders.

5.19.8 Clinical Signs in Animals

The disease is responsible for production lossesin animals.

5.19.9 Diagnosis

The disease can be diagnosed using identifica-tion of eggs followed by faecal culture so as toidentify larvae for species differentiation.

5.19.10 Control

For prevention and control of the disease, pas-ture management, stock rotation and regularde-worming of animals particularly in endemicareas should be practised. For human beings,improved personnel and environmental hygienecan help to prevent the disease.

5.20 Trichuriasis of Animal Origin

Order: EnoplidaSuperfamily: TrichuroideaFamily: Trichridae

5.20.1 Common Name/Synonyms

Whipworm disease, trichocephaliasis

5.20.2 Etiology

The zoonotic trichuriasis occurs due to Trichurisvulpis and Trichuris suis which can be occa-sionally present in intestine of man. Rarely,T. vulpis is responsible for causing VLM in man.T. vulpis primarily infects domestic and wildcanids, whereas T. suis causes infection indomestic pigs and wild boars. T. trichuria isanother parasite which could cause infection inman (Acha and Szyfres 2003).

5.19 Trichostrongylosis 109

5.20.3 Epidemiology

Both the parasites are distributed across theglobe. Malnourished 5–6 year old children intropical areas are at high risk of being infected(Márquez-Navarro et al. 2012).

5.20.4 Reservoir

Dogs, wild canids and swine could act asimportant reservoirs of infection.

5.20.5 Transmission

Trichuriasis of animal origin is a soil transmittednematode infection. The infection is transmitteddirectly through faecal oral route due to con-taminated soil or water.

5.20.6 Life Cycle

The animal or human host becomes infected afteringestion of infective eggs. After gastric passage,larvae are released in the small intestine from theseeggs. First stage larva reaches the large intestineand after multiple moults develops into the adults.

5.20.7 Clinical Signs in Man

The disease is mostly asymptomatic but diar-rhoea, dysentery, rectal prolapse, abdominalpain, vomiting, headache etc. may be seen inheavy infections.

5.20.8 Clinical Signs in Animals

The disease is generally asymptomatic but heavyinfections can cause symptoms related to gas-trointestinal system, such as diarrhoea and sec-ondary disease complications.

5.20.9 Diagnosis

The disease can be diagnosed by identificationof eggs in the faeces of the host.

5.20.10 Control

Improved personnel and environmental hygiene,proper disposal of excreta, hand washing, con-sumption of hygienic food and water can help toprevent the infection in children.

5.21 Visceral Larva Migrans

Order: AscarididaSuperfamily: AscaridoideaFamily: Ascarididae

Beaver et al. (1952) for the first time reportedmigration of Toxocara larvae to the liver. Afterthat, many cases of these larvae migrating toliver, lungs and other visceral organs have beenreported (Inoue et al. 2002; Roig et al. 1992;Morimatsu et al. 2006).

5.21.1 Common Name/Synonyms

Toxocariasis, Toxocarosis, Larval granulomato-sis, OLM.

5.21.2 Etiology

The human disease occurs due to the larvae ofToxocara sp. roundworms. The human diseaseoccurs due to Toxocara canis and T. cati. In addi-tion to these, T. vitulorum has also been recognisedas rare cause of this zoonosis. The zoonoticpotential of T. pteropodis is being questioned.T. canis toxocariasis is considered to be moreimportant than T. cati infections. For T. canis, dogsand some other canids act as definitive host,whereas cats act as definitive host for T. cati.

110 5 Nematode Zoonoses

5.21.3 Epidemiology

The disease is distributed across the globe andeggs have been found in soil from most parts ofthe world. High seroprevalences have beenrecorded from tropical countries.

5.21.4 Reservoir

Dogs act as important reservoir for humaninfections.

5.21.5 Transmission

The parasite normally affects young childrenafter accidental ingestion of infective eggs fromcontaminated soil, unwashed hands, contami-nated food and water or through ingestion of rawor undercooked tissues (particularly liver). Theinfection occurs through contamination of soiland direct contact with pets is not likely to causeinfection in human beings. Occurrence of casesafter ingestion of meat from quails, cows andchickens (Sakakibara et al. 2002) suggests itsimportance as food-borne parasitic zoonosis.

5.21.6 Life Cycle

The adult parasite sheds un-embryonated eggs inthe faeces of the definitive host. The eggs becomeinfective to third stage larvae within 7–14 days inthe environment under favourable conditions.The larvae enter the host through ingestion ofthird stage larvae present in the contaminated soilor water. The larvae hatch in the digestive systemand migrate towards the liver and then dissemi-nate to other organs, such as lungs and heart (Mok1968; Woodruff 1970). In definitive hosts, somelarvae again reach intestine through lungs anddevelop into adult worms and start releasing theeggs. For kittens, T. cati toxocariasis is nottransmitted in utero but can be transmittedthrough milk or colostrum (Fig. 5.9).

5.21.7 Clinical Signs in Man

The disease is generally not symptomatic.Clinical symptoms in man can be discussedunder four different forms viz. visceral or sys-temic, ocular, neural and covert toxocariasis(Acha and Szyfres 2003). In visceral form,symptoms could vary from asymptomatic tochronic eosinophilia, hepatomegaly, pneumoni-tis, fever and digestive disorders (Acha andSzyfres 2003). The ocular form could lead tovariety of symptoms such as retinal granulomas,retinal detachment, Keratitis and can cause lossof vision and blindness. Neurological form maylead to meningoencephalitis. The covert form isnot uncommon, and may produce symptomssuch as malaise, abdominal pain and eosino-phillia (Acha and Szyfres 2003).

5.21.8 Clinical Signs in Animals

Adult cat and dogs generally do not showsymptoms for the disease. Young puppies andkittens may show symptoms such as diarrhoea,vomiting and other digestive disturbances.

5.21.9 Diagnosis

The human infections can be diagnosed based onclinical signs, ophthalmoscopic examination,eosinophilia, other clinical pathology findings,serological tests, histologically or isolation oflarva (Aragane et al. 1999). The disease in ani-mal hosts can be diagnosed by detection of theeggs.

5.21.10 Control

For prevention and control, regular de-wormingof definitive hosts, especially their puppies andkittens must be done. Health education of per-sons in close contact with these animals shouldalso prove helpful.

5.21 Visceral Larva Migrans 111

5.22 Zoonotic Ancylostomiasis

Order: StrongylidaSuperfamily: AncylostomatoideaFamily: Ancylostomatidae

5.22.1 Common Name/Synonyms

Hookworm disease, necatoriasis, uncinariasis

5.22.2 Etiology

The disease occurs due to A. ceylanicum (catnematode) and A. caninum (dog nematode).

5.22.3 Epidemiology

Human infections are rare but have beenreported from many parts of the world. Theseparasites are endemic in India (Traub et al.2007, 2008, 2004) and south East Asia (Chooet al. 2000; Setasuban et al. 1976; Yoshidaet al. 1968). Detailed publications on humanancylostomiasis due to A. ceylanicum werepublished between the mid 1960s and early1970s (Anten and Zuidema 1964; Areekul et al.1970; Chowdhury and Schad 1972; Yoshidaet al. 1968). Recent studies by Ngui et al.(2012), Traub et al. (2008) revealed using thecombination of epidemiological, conventionaldiagnostic and molecular tools that A. ceylanicumis common in endemic areas particularly where

Fig. 5.9 Life cycle of Toxocara canis

112 5 Nematode Zoonoses

there is close contact between human and cat, dogpopulations. A. caninum is responsible for humaneosinophilic enteritis (EE) and has been reportedfrom Australia (Loukas et al. 1992; Croese et al.1994a; Landmann and Prociv 2003), UnitedStates (Khoshoo et al. 1995), Egypt (Bahgat et al.1999), Philippines, South America and Israel(Croese et al. 1994b). A. ceylanicum is able toproduce patent infections in human beings bothnaturally and experimentally (Ngui et al. 2012;Wijers and Smit 1966; Carroll and Grove 1986).Human infections due to A. ceylanicum have alsobeen reported from West New Guinea (Anten andZuidema 1964), Philippines (Velasquez andCabrera 1968), Taiwan (Yoshida et al. 1968),Thailand (Areekul et al. 1970; Traub et al. 2008;Jiraanankul et al. 2011), Laos (Sato et al. 2011)and India (Chowdhury and Schad 1972).

5.22.4 Reservoir

Dogs can act as reservoir hosts for humanhookworm infections.

5.22.5 Transmission

Ingestion of contaminated soil or food like veg-etables could transmit infection in human beings.

5.22.6 Life Cycle

The parasite A. ceylanicum has a direct life cycle.This parasite is present in small intestine of dogs,cats and humans. The infection occurs due toingestion or percutaneous migration of infectiousthird stage larvae from the soil. The host animalpasses un-embryonated eggs in the faeces after14 days of entry into the host (Yoshida et al.1974). The infectious larvae usually develop in2–8 days under favourable conditions.

5.22.7 Clinical Signs in Man

A. ceylanicum can develop into adult in humanbeings (Tu et al. 2008; Anten and Zuidema1964) and produces natural patent infectionscausing anaemia (Anten and Zuidema 1964;Velasquez and Cabrera 1968; Chowdhury andSchad 1972; Traub et al. 2008). A. caninumoccasionally reaches adulthood in humans(Landmann and Prociv 2003; Prociv and Croese1990; Croese et al. 1994a, b) and can causeeosinophilic enteritis (Prociv and Croese 1996).

5.22.8 Clinical Signs in Animals

Heavy infections due to A. ceylanicum can causediarrhoea, bloody and mucoid stool and irondeficiency anaemia (Carroll and Grove 1984) indogs. Migrating larva in heavy infections canaffect and cause symptoms in cutaneous, respi-ratory and intestinal systems.

5.22.9 Diagnosis

The disease can be diagnosed by identificationof parasite eggs, from clinical signs in animalssuch as anaemia (pale mucus membranes), roughhair coat, by use of serological tests such asELISA, western blot and molecular techniques(Sato et al. 2010).

5.22.10 Control

Control measures for non-zoonotic humanancylostomiasis such as prophylactic and thera-peutic treatment and improved sanitation foranimals also work well for control of zoonoticancylostomiasis.

5.22 Zoonotic Ancylostomiasis 113

5.23 Zoonotic Filariasis

Order: SpiruridaSuborder: FilariinaSuperfamily: Filariroidea

5.23.1 Common Name/Synonyms

Brugia malayi filariasis

5.23.2 Etiology

Many species of animal filariasis are reported tocause disease in man (Addario 1885; Gutierrez1990; Orihel and Ash 1995).

Zoonotic filariasis could primarily occur dueto the following etiological agents:1. Dirofilaria spp. viz. D. immitis, D. tenuis,

D. repens2. Onchocerca spp. viz. O. cervicalis,

O. gutturosa3. Brugia spp. viz. B. malayi, B. pahangi,

B. leporis4. Other species such as Loaina sp., Meningo-

nema sp., and some unidentified species

5.23.3 Epidemiology

Cases due to zoonotic filariasis have beenreported across the globe (Orihel and Eberhard1998; Thomas and Mark 1998). Zoonotic filari-asis has been reviewed in detail by Orihel andEberhard (1998). Different species of Brugiainfect animals such as tree shrews and monkeysin Southeast Asia, and raccoons and rabbits inthe United States (Eberhard 1984; Orihel 1966;Orihel and Pacheco 1966). Human infectionsdue to D. repens have been reviewed byPampiglione et al. (1995) and reported 400 casesfrom 30 countries in Europe, Asia and Africa.Most human infections have been reported fromtemperate zones (Orihel and Eberhard 1998).

5.23.4 Reservoir

Monkeys, cats and wild carnivores act as reser-voir for subperiodic brugiasis in Southeast Asia(Acha and Szyfres 2003). Other wild anddomestic animals might also act as reservoirs forthe disease.

5.23.5 Transmission

The disease is transmitted by the bite of bloodsucking insects such as mosquitoes belonging tothe genra Mansonia.

5.23.6 Life Cycle

Zoonotic filariasis is a vector borne disease andblood sucking insects act as biological vectors fortransmissionof thedisease.Theadultparasite livesin vertebrate host’s tissues. The female releasesembryos (microfilariae) which can be found inblood, lymph or skin. The vectors transmit theinfection by feeding previously on an animalinfected with a patent filaria infection (Anderson1992). The arthropod vector ingests microfilariaepresent in blood, lymph or skin. The microfilariaefurtherdevelopinto infectious thirdstage larvaandmigrate towards the mouthparts of the arthropod.The insect vector then transmits the infectionwhile feeding on another new vertebrate host.

5.23.7 Clinical Signs in Man

Brugia spp. infects lymphatic system and pro-duces symptoms such as lymphadenopathy andlymphangitis. Dirofilaria spp. generally infectsskin and subcutaneous tissue and produce rela-ted symptoms such as nodules and swellings.D. immitis can infect heart, pulmonary and otherblood vessels and produce related symptoms.

114 5 Nematode Zoonoses

5.23.8 Clinical Signs in Animals

The disease is generally asymptomatic but largenumber of parasites could pose problems such asstenosis of pulmonary vessels, obstruction in flowof blood.

5.23.9 Diagnosis

Blood smear examinations and Millipore filterconcentration techniques, PCR, ELISA can beused for diagnosis of parasites present in thehuman blood.

5.23.10 Control

Control of vector populations can help preventand control these infections.

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122 5 Nematode Zoonoses

6Arthropod Zoonoses

Abstract

Arthropod Zoonoses could be defined as ‘‘those arthropod diseases whichare naturally transmitted between (other) vertebrate animals and man’’.Infestation of dipteran fly larva could cause myiasis in animals and man.Pentastomiasis is a zoonotic disease which can occur in human beings.The disease occurs due to Armillifer and Linguatula species (FamiliesPorocephalidae and Linguatulidae); endoparasites of reptiles, birds andmammals. Tungiasis occurs due to the infestation of female sand fleaTunga (Sarcopsylla) penetrans and could result in tungiasis in dogs, cats,pigs, non-human primates and occasionally man. Tungiasis has beenreported from many countries. Zoonotic scabies occurs due to Sarcoptesscabiei which affects many mammal and marsupial species.

6.1 Myiasis

Class: InsectaOrder: Diptera

The disease occurs due to dipteran fly larvawhich infests live vertebrates viz. animals andhumans (Zumpt 1965). These larvae feed on theliving/dead tissue/body fluids of the host or oningested food (Francesconi and Lup 2012). Thelarvae can infest different locations and producespectrum of symptoms depending upon the lar-vae species and the host involved (Noutsis andMillikan 1994; Francesconi and Lup 2012).

6.1.1 Etiology

Although many species can cause the disease,the important etiological agents include:

6.1.1.1 Specific Parasites• Larvae of Cochliomyia hominivorax (screw

worm)• Larvae of Chrysoma bezziana• Furuncular myiasis due to larva of Cordylobia

anthropophaga• Furuncular myiasis due to larvae of Derma-

tobia hominis• Furuncular myiasis due to Cuterebra spp.• Larvae of Hypoderma spp.• Larvae of Oestrus ovis and Rhinoestrus

purpureus• Larvae of Gasterophilus spp.• Furuncular myiasis due to Wohlfahrtia spp.

6.1.1.2 Facultative or Semi SpecificMyiasis

• Due to larvae of Lucilia sericata, Sarcophaga,Parasarcophaga, Phormia, Paraphrominaspecies

B. B. S. Dhaliwal and P. D. Juyal, Parasitic Zoonoses,DOI: 10.1007/978-81-322-1551-6_6, � Springer India 2013

123

6.1.1.3 Accidental Myiasis• Due to larvae of Musca domestica, Musca

stabulans, Fannia canicularis, F. scalaris

6.1.2 Epidemiology

The disease is worldwide in distribution. Highprevalence has been recorded from poor socio-economic regions of tropical and subtropicalcountries (Francesconi and Lup 2012). Animalsplay an important role and man generally acts asan accidental host. Poor hygiene and lowsocioeconomic status are the important risks forthe occurrence of the disease (Fernandes et al.2009; Marquez et al. 2007).

6.1.3 Clinical Signs in Animals

Myiasis could lead to severe production lossessuch as reduced milk yield, inferior quality ofhide, decreased weight and fertility losses(Francesconi and Lup 2012).

6.1.4 Clinical Signs in Man

Depending upon symptoms, human myiasis hasbeen discussed under following headings.

6.1.4.1 Cutaneous MyiasisThis is most frequently encountered form ofmyiasis (Diaz 2009).1. Furuncular myiasis: It occurs when dipteran

larvae penetrate healthy skin. Symptomsinclude erythematous, furuncle-like nodulecontaining one or more maggots in it. It mainlyoccurs due to Dermatobia hominis andCordylobia anthropophaga. Important clinicalsymptoms include pruritus, pain, and move-ment sensation (Mahal and Sperling 2012).

2. Migratory (creeping) myiasis: It occurs dueto aimless migration of dipteran larvathrough burrows in the skin. It producesmigratory patterns of the lesions. Clinical

symptoms include painful and migratoryswelling.

3. Wound myiasis: It results due to local tissuedestruction and further invasion into deeptissues.

6.1.4.2 Cavitary MyiasisCavitary myiasis occurs due to infestation ofbody cavities by the larvae. The symptoms varydepending upon the cavity or organ affected orinvolved. For example in ophthalmomyiasis,important clinical symptoms include vision lossand eye pain.

6.1.5 Diagnosis

The disease can be diagnosed from clinicalsigns, ultrasound examination or by detection ofthe larva.

6.1.6 Control

Improved personnel and environmental sanita-tion, measures for control of flies, maggot ther-apy and reducing animal myiasis can helpcontrol the infection.

6.2 Pentastomiasis

Class: PentastomidaFamily: Porocephalidae

6.2.1 Common Name/Synonyms

Porocephaliasis, Tongue worm infection, golfcaddy’s disease, halzoun, marrara

6.2.2 Etiology

Pentastomiasis is a zoonotic disease whichcan infect human beings. These parasites are

124 6 Arthropod Zoonoses

endoparasites of reptiles, birds and mammals.The disease occurs due to parasites belonging tofamilies Porocephalidae and Linguatulidae viz.Armillifer and Linguatula species. The diseasecan occur in two forms viz. visceral or naso-pharyngeal pentastomiasis. The visceral formoccurs when humans ingest infective eggs ofArmillifer armillatus or L. serrata and act asintermediate host.

Nasopharyngeal pentastomiasis occurs whenman ingests raw or undercooked infected inter-mediate host (e.g. sheep or goat) containingencysted nymphs of the parasite L. serrata.

6.2.3 Epidemiology

The disease is worldwide in distribution withmany reports from Asia and tropical Africa.A. armillatus is primarily found in Africa whereashuman cases due to L. serrata have been reportedfrom North Africa, Europe and Middle East(Acha and Szyfres 2006; Aynimode et al. 2010).Pentastomiasis among humans in China havebeen found to be associated with the ingestion ofraw or undercooked snakes (Min et al. 2008).

6.2.4 Transmission

Vertebrate animals including primates andhumans act as intermediate hosts (Lang et al.1987). Human beings become infected either afterconsumption of contaminated water or vegetablescontaminated by faeces of definitive host or due tothe naso bronchial secretions of infected snakes orcarnivores, or by eating raw or undercooked snakeor lizard (Machado et al. 2006).

6.2.5 Life Cycle

For Armillifier species, snakes act as definitivehosts and rodents and other wild mammals act asintermediate hosts. For Linguatula spp., herbiv-orous animals such as sheep, goat act as inter-mediate hosts and dogs, canids and some felids

act as definitive hosts. Intermediate hosts becomeinfected after the ingestion of the egg containedeither in faeces or in the sputum of the definitivehosts. The eggs develop to larva in the interme-diate host and then burrow towards the abdominalcavity. Larvae mature to nymphs and remain inthe viscera in an encysted form. Definitive hostsbecome infected after consumption of the inter-mediate host containing the encysted nymphs.

6.2.6 Clinical Signs in Man

The disease is generally not symptomatic butcould produce symptoms when encysted larvaeenlarge through molting and cause pressure orduring larval migration in vital organs. There arereports of vital organ collapse viz. lung (Stock1946), intestinal obstruction (Cannon 1942),peritonitis (Herzog et al. 1985) and glaucoma(Lang et al. 1987). Liver is another commonlyaffected organ.

6.2.7 Clinical Signs in Animals

In definitive hosts, Linguatula infections couldproduce symptoms such as nasal catarrah,sneezing and epistaxis (Acha and Szyfres 2006).In general, the infections remain asymptomaticin intermediate hosts.

6.2.8 Diagnosis

In definitive hosts, the disease can be diagnosedby the identification of the characteristic thick-shelled eggs containing an embryo with rudi-mentary legs. Intermediate host infections aredifficult to diagnose and may be diagnosed eitherby X-rays or histopathological examination.

6.2.9 Control

Improved personnel hygiene and avoid eatingraw or undercooked infected meat for preventionof the disease.

6.2 Pentastomiasis 125

6.3 Tungiasis

Order: SiphonapteraFamily: Tungidae

6.3.1 Synonyms

Chigoe, jigger flea infestation sand fleainfestation

6.3.2 Etiology

The disease occurs due to the infestation offemale sand flea Tunga (Sarcopsylla) penetrans.

6.3.3 Epidemiology

This flea could infest warm-blooded animalsincluding dogs, cats, pigs, non-human primatesand man. The disease has been reported fromCentral, South and Latin America, Caribbean,Africa and India (Leung et al. 2007).

6.3.4 Transmission

In endemic areas, human beings could becomeinfected when they walk barefoot on the soilcontaining the fleas.

6.3.5 Life Cycle

The fleas are hematophagous (Eisele et al. 2003;Fein et al. 2001) and male dies quickly after thecopulation. The female flea penetrates in thehost epidermis and lay eggs for 2–3 weeksbefore death. The eggs fall and mature intolarvae on the soil (Fein et al. 2001). The larvaedevelop to pupae and finally develop intoadult flea. The whole cycle is completed in18 days under favourable conditions (Leunget al. 2007).

6.3.6 Clinical Signs in Manand Animals

Clinical symptoms range from asymptomatic topruritic, painful ulceration having papular ornodular lesion with a central dark spot. The fleacommonly infests feet but could affect any partwhich comes in contact with the soil (Leunget al. 2007). The symptoms could be furtherdeteriorated with secondary bacterial infections.

6.3.7 Diagnosis

The disease can be diagnosed from clinicalsymptoms or by identification of flea fromcharacteristic lesions.

6.3.8 Control

Flea control measures, avoidance of walkingbarefoot can help prevent the infection.

6.4 Zoonotic Dermatitis

Zoonotic dermatitis occur in man primarily dueto three parasites1. Sarcoptes scabiei causing zoonotic scabies2. Tick infestations due to ticks of various

species3. Other acarid parasites such as parasites of the

families Cheyletiellidae, Dermanyssidae andMacronyssidae

6.4.1 Zoonotic Scabies

Phylum: ArthropodaClass: ArachnidaFamily: Sarcoptidae

6.4.1.1 Common Name/SynonymsAcariasis, Mange, sarcoptic itch

126 6 Arthropod Zoonoses

6.4.1.2 EtiologyThe disease occurs due to Sarcoptes scabieiwhich affects many mammal and marsupialspecies. There are many subtypes of the parasitewhich could be host specific. Important subtypesinclude S. scabiei var hominis which primarilyinfect humans, S. scabiei var. canis, S. scabieivar bovis, S. scabiei var. equi, S. scabiei var suisand S. scabiei var ovis. Humans could alsobecome infected by many of these subtypes. Inaddition to these, humans can also becomeinfected with Notoedres cati (notoedric mange)present in cats and Trixacarus caviae (guineapig mite) affecting guinea pigs.

6.4.1.3 EpidemiologyThe parasite S. scabies is worldwide in distri-bution. Human disease particularly occurs inpersons belonging to poor and lower socioeco-nomic groups.

6.4.1.4 TransmissionHuman beings become infected either throughdirect contact with infected animal or by indirectcontact with fomites (Arlian et al. 1984).

6.4.1.5 Life CycleThe parasite burrows tunnels in the skin andlives there. The parasite completes its life cycleon the host skin and cannot survive in theenvironment for long period of time. Males dieafter copulation. The female form tunnels in theskin and lay eggs. The larvae hatch and migratetowards the surface of the skin. Larvae furthermolt to nymphal and adult parasite.

6.4.1.6 Clinical Signs in ManHuman cases due to S. scabiei var. canis havebeen reported (Arlian et al. 1984; Weese et al.2002). Zoonotic scabies is generally a self lim-iting disease in human beings. In humans, theparasite may cause intense pruritus commonlyaffecting arms, legs, thoracic and abdominal

regions. The zoonotic infections normally do notcause burrows and produce symptoms such asdermatitis, vesicles and papules.

6.4.1.7 Clinical Signs in AnimalsClinical symptoms in animals include intensepruritus and are commonly found on legs, faceand trunk (Arlian et al. 1984).

6.4.1.8 DiagnosisThe disease can be diagnosed from clinical signsand identification of the mite from the lesions.

6.4.1.9 ControlPrevention and control of the parasite in animalsand using protective measures can help preventinfection in human beings.

6.4.2 Tick Infestations

Class: ArachnidaOrder: Acarina

6.4.2.1 FamilyArgasidae (soft ticks) and Ixodidae (hard ticks)

6.4.2.2 EtiologyMany species can cause tick infestations in man.There are approximately 12 argasid (Argasand Ornithodos), 20 ixodid (4 Amblyomma,7 Dermacentor species, 3 Haemaphysalis spe-cies, 2 Hyalomma species and 6 Ixodes species)tick species which can infest man (Estrada-Penand Jongejan 1999). The detailed reviews ontick infestations in human beings are available inthe literature (Estrada-Pen and Jongejan 1999).

6.4.2.3 EpidemiologyThe ticks are distributed across the globevarying with species and regions. Many human

6.4 Zoonotic Dermatitis 127

cases have been recorded in the literature(Estrada-Pen and Jongejan 1999).

6.4.2.4 TransmissionInfected animals shed adult or larvae in theenvironment from where they can infect humanbeings.

6.4.2.5 Clinical Signs in ManAccidental infections normally occur in humanbeings. Tick infestations could lead to paralyses,toxicities and allergic reactions (Estrada-Pen andJongejan 1999; Gauci et al. 1989). Additionally,ticks can also transmit many important vectorborne zoonotic diseases in animals and man(Sonenshine 1991). Paralysis due to bite ofOtobius megnini (Peacock 1958), ear infesta-tions (Chellappa 1973), allergic reactions (Gauciet al. 1989), irritation (Eads and Campos 1984;Uilenberg et al. 1980) and toxic reactions fol-lowing the bites of A. brumpti and O. moubata(Sonenshine 1993) have been reported.

6.4.2.6 Clinical Signs in AnimalsClinical symptoms are generally similar as inman. Additionally, ticks can transmit manyimportant vector borne zoonotic diseases inanimals and man (Sonenshine 1991).

6.4.2.7 DiagnosisThe disease can be diagnosed by removal andidentification of tick species involved.

6.4.2.8 ControlImproved personnel habitat and control of ticksin animals can help prevent human infections.

6.4.3 Dermatitis Due to AcaridParasites Belonging to FamiliesCheyletiellidae, Dermanyssidaeand Macronyssidae

Class: ArachnidaOrder: Acarina

6.4.3.1 Etiology

1. Cheyletiella parasitovorax (rabbit parasite),C. yasguri (dog parasite) and C. blakei (catparasite)

2. Dermanyssus gallinae (chicken, turkeys,pigeons, canaries, wild fowl parasite)

3. Liponyssoides sanguineus (small rodentparasite)

4. Ornithonyssus bacoti (rodents and small mar-supials parasite), O. bursa and O. sylvarium(birds parasite)

6.4.3.2 EpidemiologyMost of these mites are worldwide indistribution.

6.4.3.3 TransmissionClose contact with respective animal hosts isresponsible for transmission of the disease.

6.4.3.4 Life CycleThe female mite lays eggs in burrows, nests orcracks or attached to animal hairs dependingupon the host involved. These eggs hatch andrelease larvae which further develop to becomeadults.

6.4.3.5 Clinical Signs in ManThe primary sign is dermatitis and parasite mayinfect different body parts such as thorax, arms,thighs, etc. Bite of these mites could producesevere symptoms such as intense pruritis, aller-gic dermatitis, urticaria and skin irritationdepending upon the species involved (Acha andSzyfres 2003).

6.4.3.6 Clinical Signs in AnimalsIn the animal hosts, symptoms such as dandruff,alopecia, pruritis, scaly condition, anemiaand irritation could be seen varying upon thehost and species involved (Acha and Szyfres2003).

128 6 Arthropod Zoonoses

6.4.3.7 DiagnosisIdentification of causative agents using micro-scopic or skin scrapings can help diagnose thedisease.

6.4.3.8 ControlThe infected animals should be properly treatedwith acaricides (Acha and Szyfres 2003).

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6.4 Zoonotic Dermatitis 129

About the Authors

Dr. B. B. Singh DhaliwalDr. Balbir Bagicha Singh Dhaliwal (Ph.D.) isworking as Assistant Professor (VeterinaryPublic Health) with Guru Angad Dev Veterinary& Animal Sciences University’s School ofPublic Health & Zoonoses (Ludhiana, India). Heparticipated as Visiting Scientist at Centre forFood Borne & Animal Parasitology, OIE Ref-erence Lab (Trichinella) & Collaborating Centre(Food Borne & Zoonotic Parasites), CanadianFood Inspection Agency, Saskatoon (Canada)for a period of six months. He is working in thefield of Food Borne & Zoonotic Parasitologysince the last 13 years. He is a recipient of Dr.V. S. Alwar memorial award (2004), TheFlemish Vlaamse Interuniversitaire Raad—Uni-versity Development Corporation (VLIR–UOS)grant (2007) and the World Association forAdvancement of Veterinary ParasitologyScholarship funding (2013). He has severalresearch publications in the field of Food Borne& Zoonotic Parasitology in international andnational journals of repute.

Dr. P. D. JuyalDr. P.D. Juyal served at RAU, Pusa (Bihar),GBPU&T, Pantnagar and PAU, Ludhiana and as

Professor and Head Department of VeterinaryParasitology at Guru Angad Dev Veterinary &Animal Sciences University, Ludhiana (India).Presently, Dr. Juyal is working as Registrar,GADVASU, Ludhiana (India). He has publishedmore than 189 research and extension papersand six practical manuals for UG students. He isEx-Vice-President of Indian Society for Parasi-tology and General Secretary of Indian Associ-ation for Advancement of VeterinaryParasitology (IAAVP). He is national fellow ofIAAVP and fellow of National Academy ofVeterinary Sciences (NAVSc). He is also amember of the editorial board of Journal ofParasitic Diseases, Journal of Laboratory Phy-sicians (New Delhi), and Pakistan J. Vet. &A. Sc. (Lahore). Besides, he is also a nominee/representative of CPCSEA for many pharmacycolleges in Punjab. He is a recipient of the Prof.B.V. Rao Gold Medal (1998) for research pub-lications in journals.

B. B. S. Dhaliwal and P. D. Juyal, Parasitic Zoonoses,DOI: 10.1007/978-81-322-1551-6, � Springer India 2013

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Index

AAcanthocephalus, 83Accidental myiasis, 124African trypanosomosis, 15Amebiosis, 17Amphixenosis, 3Ancylostoma braziliense, 92Ancylostoma caninum, 92Ancylostoma ceylanicum, 92Ancylostoma tubaeforme, 92Angiostrongylosis, 85Angiostrongylus cantonensis, 85Anisakiosis, 86Anisakis, 87Anthropozoonoses, 3Argas, 127Armillifer, 125Armillifer armillatus, 125Ascariosis, 88Ascaris lumbricoides, 88Ascaris suum, 88Atypical human trypanosomosis, 35Austrobilharzia, 42

BBabesia divergens, 19Babesia microti, 19Babesiosis, 19Balantidiosis, 21Balantidium coli, 21Baylisascariasis, 89Baylisascaris procyonis, 89Bertiellosis, 78

CCapillaria aerophila, 91Capillaria hepatica, 91Capillaria philippinensis, 91Capillariasis, 91Corynebacterium bovis, 76

Cattle related parasitic zoonoses, 3Cercarial dermatitis, 41Chagas disease, 21Cheyletiella parasitovorax, 128Chrysoma bezziana, 123Classification of parasitic zoonoses, 2Clonorchiosis, 52Clonorchis sinensis, 52Cochilomyia hominivorax, 123Coenurosis, 63Coenurus brauni, 66Coenurus cerebralis, 63Coenurus serialis, 63Contracaecum, 87Cordylobia anthropophaga, 123, 124Cryptosporidiosis, 22Cryptosporidium parvum, 22Cutaneous larva migrans, 92Cutaneous Leishmaniosis, 28Cyclospora cayetanensis, 33Cyclosporosis, 33Cyclozoonoses, 3Cysticercus cellulosae, 76

DDermacentor, 127Dermanyssus gallinae, 128Dermatobia hominis, 124Dendritobilharzia, 42Dicrocoeliasis, 43Dicrocoelium dendriticum, 44Dioctophyma renale, 93Dioctophymosis, 93Diphyllobothriosis, 67Diphyllobothrium, 67Diphyllobothrium hospes, 43Diphyllobothrium latum, 67Diphyllobothrium nihonkaiense, 67Dipylidiosis, 68Dipylidium caninum, 69Direct parasitic zoonoses, 2

B. B. S. Dhaliwal and P. D. Juyal, Parasitic Zoonoses,DOI: 10.1007/978-81-322-1551-6, � Springer India 2013

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Dracunculiasis, 94Dracunculus medinensis, 95

EEchinochasmus japonicus, 45Echinococcus, 71Echinostoma hortense, 45Echinococcus echinatum, 45Echinococcus granulosus, 71Echinococcus multilocularis, 71, 72Echinococcus oligarthrus, 71, 72Echinococcus vogeli, 71, 72Echinococcosis, 71Echinostomosis, 45Entamoeba histolytica, 17Entamoeba polecki, 17

FFannia canicularis, 124Fasciola gigantica, 46Fasciola hepatica, 46Fasciolopsiosis, 47Fasciolopsis buski, 48Fasciolosis, 46Fish related parasitic zoonoses, 3Fish, shellfish and mollusc borne parasitic

zoonoses, 6Food borne parasitic zoonoses, 9

GGastrodiscoides hominis, 49Gastrodiscoidosis, 49Giardia intestinalis, 25Giardiosis, 25Gigantobilharzia, 42Gnathostoma, 96Gnathostoma nipponicum, 96Gnathostoma spinigerum, 96Gnathostomosis, 96Gongylonema pulchrum, 97Gongylonemosis, 97

HHaemaphysalis, 127Halicephalobus gingivalis, 101Haplorchiosis, 51Heterophyosis, 49Heterophyosis due to Heterophyes species, 50Hymenolepiosis, 79

IInermicapsiferosis, 79Infections caused by free-living amoebae, 33

LLagochilascariosis, 99Lagochilascaris, 99Leishmania, 28Leishmania braziliensis, 28Leishmaniasis donovani, 27Leishmaniasis infantum, 27Leishmaniasis major, 99Leishmaniasis mexicana, 28Leishmaniasis minor, 99Leishmaniasis sprenti, 99Leishmaniasis tropica, 28Leishmaniasis turgida, 99Leishmaniosis, 26Linguatula, 124Linguatula serrata, 124Liponyssoides sanguineus, 128Livestock related parasitic

zoonoses, 4

MMalaria in nonhuman primates, 35Mammomonogamus, 100Mammomonogamus laryngeus, 100Meat borne parasitic zoonoses, 10Mesocestoidosis, 79Metagonimosis, 49Metagonimus miyatai, 49Metagonimus takahashii, 49Metagonimus yokogawai, 49Metazoonoses, 3Metorchiosis (Canadian liver fluke), 53Micronema deletrix, 101Micronemosis, 101Microsporidiosis, 35Milk borne parasitic zoonoses, 12Musca domestica, 124Myiasis, 124

NNanophyetosis, 51Nanophyetus salmincola, 51Nanophyetus schikhobalowi, 51

OOccupational parasitic zoonoses, 7Oesophagostomiasis aculeatum, 102Oesophagostomiasis, 102Oesophagostomum bifurcum, 102Opisthorchiosis, 52Ornithodos, 127Ornithonyssus bacoti, 128Other cestode zoonoses, 78Other Liver flukes, 52Other Metagonimus species, 50

134 Index

PParagonimosis, 53Paragonimus westermani, 54Parasitism, 1Pentastomiosis, 124Pet animal related parasitic zoonoses, 5Pig related parasitic zoonoses, 3Poultry related parasitic zoonoses, 13Pseudoterranova, 87

RRaillietinosis, 79Raw vegetables/plant borne parasitic zoonoses, 13Reptile, amphibian borne parasitic zoonoses, 13Rhinoestrus purpureus, 123

SSarcocystiosis, 30Sarcoptes scabiei, 126Sarcocystis hominis, 30Sarcocystis miescheriana, 30Sarcocystis suihominis, 30Saprozoonoses, 3Schistosoma japonicum, 56Schistosoma malayi, 56Schistosoma mansoni, 56Sheep related parasitic zoonoses, 3Soil transmitted parasitic zoonoses, 13Spirometra erinaceieuropaei, 74Sparganosis, 74Spirometra mansoni, 74Spirometra mansonoides, 74Strongyloides fuelleborni, 103Strongyloides stercoralis, 103Strongyloidiasis, 103

TTaenia axei, 108Taenia serialis, 66Taenia solium, 76Taeniidae saginata, 76Taeniosis and cysticercosis, 76Ternidens derminutus, 102Thelazia callipaeda, 105Thelaziidae californiensis, 105Thelaziidae callipaeda, 105Thelaziidae rhodesii, 105Thelaziasis, 104Tick Infestations, 127Toxocara, 110Toxocara canis, 110

Toxocara cati, 110Toxocara pteropodis, 110Toxocara vitulorum, 110Toxoplasma gondii, 32Toxoplasmosis, 32Trematosaurus brauni, 66Trichinella, 106Trichinella multiceps, 66Trichinella murrelli, 106Trichinella nativa, 106Trichinella nelsoni, 106Trichinella papuae, 106Trichinella psudospiralis, 106Trichinella spiralis, 106Trichinella britovi, 106Trichinosis, 105Trichobilharzia, 42Trichostrongylosis, 108Trichostrongylus brevis, 108Trichostrongylus capricola, 108Trichostrongylus colubriformis, 108Trichostrongylus orientalis, 108Trichostrongylus probolurus, 108Trichostrongylus skrjabini, 108Trichostrongylus vitrinus, 108Trichuriosis of animal origin, 109Trichuris suis, 109Trichuris vulpis, 109Trypanosoma cruzi, 21Trypanosomatidae brucei gambiense, 16Trypanosomatidae brucei rhodesiense, 16Tunga (Sarcopsylla) penetrans, 126Tungosis, 126

VVector borne parasitic zoonoses, 13Visceral larva migrans, 110Visceral Leishmaniosis, 27

WWater borne parasitic zoonoses, 11Wildlife related parasitic zoonoses, 4Wohlfahrtia spp, 123

ZZooanthroponoses, 3zoonoses, 1Zoonotic ancylostomiasis, 112Zoonotic dermatitis, 126Zoonotic filariasis, 114

Index 135